Affinage

ICAM3

Intercellular adhesion molecule 3 · UniProt P32942

Length
547 aa
Mass
59.5 kDa
Annotated
2026-06-10
100 papers in source corpus 40 papers cited in narrative 39 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ICAM-3 (CD50/ICAM-R) is a five-domain immunoglobulin-superfamily adhesion molecule constitutively expressed on resting leukocytes that serves as a principal ligand for the integrin LFA-1 (CD11a/CD18) and acts as a bidirectional signaling and adhesion hub at leukocyte contact sites (PMID:1448173, PMID:1448174, PMID:7905020). LFA-1 binding is mediated by the N-terminal Ig-like domain 1, which is necessary and sufficient, through residues clustering on both the ABED and GFC faces — a more extensive footprint than that used by ICAM-1 — and is engaged through the LFA-1 α-subunit I domain in a cation-dependent manner (PMID:8798624, PMID:9686599, PMID:7518468, PMID:9271587). Beyond LFA-1, ICAM-3 is preferentially bound by the αdβ2 integrin and, via Lewis-x and high-mannose glycans on its complex-type N-linked oligosaccharides, by the dendritic-cell lectin DC-SIGN to mediate early DC–T-cell adhesion (PMID:8777714, PMID:10721994, PMID:17145745, PMID:11179968). ICAM-3 engagement triggers outside-in signaling: it associates with the Src-family kinases p56lck and p59fyn, drives calcium flux and tyrosine phosphorylation under CD45 regulation, raises β1/β2 integrin avidity, and co-stimulates T-cell proliferation and chemokine secretion from monocytes and neutrophils (PMID:7515097, PMID:7520448, PMID:7515813, PMID:8223855, PMID:9605163, PMID:9834117). The molecule polarizes to the T-cell uropod and clusters at the APC contact-initiation zone, positioning it for the earliest scanning phase of immune synapse formation, and is shed proteolytically from activated neutrophils and lymphocytes to yield a circulating soluble form (PMID:7525599, PMID:11812993, PMID:7525295, PMID:7876564). On apoptotic leukocytes, domain 1–2 of ICAM-3 switches to an alternative recognition activity that tethers dying cells and their microparticles to macrophage CD14 to drive chemoattraction and efferocytosis (PMID:10352301, PMID:22117198, PMID:23775590). Its leukocyte-restricted promoter is repressed by RUNX3 during monocyte-to-macrophage differentiation (PMID:22479382). In cancer cells ICAM-3 promotes migration, invasion, stemness and metastasis through an intracellular YLPL-Src-AKT-CREB-MMP axis and an LFA-1–ICAM-3–ERM mechanical-tension mechanism (PMID:19956847, PMID:29477378, PMID:29729315).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1992 High

    Established the molecular identity of ICAM-3 as an IgSF adhesion molecule and a third constitutive LFA-1 ligand, defining a leukocyte-restricted adhesion receptor distinct from endothelial ICAMs.

    Evidence expression cloning, cell adhesion and antibody-blocking assays across two independent papers

    PMID:1448173 PMID:1448174

    Open questions at the time
    • Binding interface on ICAM-3 not yet mapped
    • Cytoplasmic signaling function unknown
  2. 1993 High

    Showed ICAM-3 is not merely an adhesive ligand but an active regulator that, when engaged, drives LFA-1/ICAM-1-dependent aggregation and co-stimulates proliferation, and confirmed CDw50/ICAM-3 identity.

    Evidence adhesion on purified ICAM-3, mAb blocking, immunofluorescence, proliferation assays, protein sequencing

    PMID:7901223 PMID:8325327

    Open questions at the time
    • Signaling intermediates downstream of engagement undefined
    • Mechanism of integrin avidity modulation unclear
  3. 1994 High

    Localized the LFA-1 binding site to ICAM-3 domain 1 by systematic mutagenesis and structural EM, defining conserved versus specificity-conferring residues and the reciprocal LFA-1 I domain as the binding partner.

    Evidence domain-deletion chimeras, 45 point mutants, mAb epitope mapping, electron microscopy

    PMID:7518468 PMID:7531103 PMID:8798624

    Open questions at the time
    • Co-crystal structure absent
    • Conformational requirements on LFA-1 not fully resolved
  4. 1994 High

    Defined ICAM-3 outside-in signaling, linking engagement to Src-family kinases, calcium flux, CD45-regulated tyrosine phosphorylation, and integrin avidity upregulation.

    Evidence anti-CD50 cross-linking, Ca2+ measurement, phosphotyrosine co-IP and in vitro kinase assays, CD45 inhibitor and tyrosine-kinase inhibitor studies, adhesion assays

    PMID:1730238 PMID:7515097 PMID:7515813 PMID:7520448 PMID:8223855

    Open questions at the time
    • Direct adaptor coupling p56lck/p59fyn to ICAM-3 cytoplasmic tail not defined
    • Whether phosphorylation is on ICAM-3 itself or associated proteins not fully resolved
  5. 1994 High

    Defined ICAM-3 receptor specificity and ligand promiscuity — it binds the new αdβ2 integrin preferentially over ICAM-1 but is not a ligand for Mac-1 or p150,95 — narrowing the set of relevant integrin partners.

    Evidence cDNA cloning of αd, transfectant adhesion comparisons, bidirectional purified-protein adhesion assays

    PMID:7737271 PMID:8777714

    Open questions at the time
    • Physiological context of αdβ2–ICAM-3 binding unclear
    • Affinity hierarchy among integrin ligands not quantified
  6. 1994 High

    Demonstrated that ICAM-3 surface levels are dynamically controlled by proteolytic shedding from activated neutrophils and lymphocytes, generating a circulating soluble form.

    Evidence internalization assays ruling out endocytosis, protease inhibition, detection of shed protein in supernatant and plasma, ELISA/immunoblot size comparison

    PMID:7525295 PMID:7876564

    Open questions at the time
    • Identity of the responsible protease not established
    • Functional role of soluble ICAM-3 in vivo unclear
  7. 1998 High

    Refined the LFA-1 binding footprint, showing it spans both ABED and GFC faces of domain 1 — more extensive and partly distinct from ICAM-1 — explaining selective ligand engagement.

    Evidence 18-residue site-directed mutagenesis with LFA-1 adhesion assays

    PMID:9686599

    Open questions at the time
    • No atomic-resolution structure of the complex
  8. 1998 High

    Established epitope-specific outside-in signaling on myeloid cells, with domain-1-directed engagement driving chemokine secretion, spreading, and β2-integrin-dependent aggregation through tyrosine and PKC kinases.

    Evidence Fab/F(ab')2 fragment engagement controls, chemokine ELISA, kinase and cytoskeleton assays, anti-β2 blocking

    PMID:9605163 PMID:9834117

    Open questions at the time
    • Direct cytoplasmic effectors transducing the signal undefined
    • Why different domain-1 mAbs give opposite effects (HP2/19 vs CAL3.10) mechanistically unexplained
  9. 1999 High

    Revealed a context switch in ICAM-3 function: on apoptotic leukocytes domain 1 changes binding preference from LFA-1 to a macrophage CD14-dependent recognition activity for clearance of dying cells.

    Evidence mAb blockade of candidate macrophage receptors, ICAM-3 transfection into non-leukocytes, multiple apoptosis stimuli

    PMID:10352301

    Open questions at the time
    • Molecular basis of the apoptotic conformational/glycan change not defined
    • Direct CD14–ICAM-3 binding not biochemically reconstituted
  10. 2000 High

    Identified DC-SIGN as a high-affinity ICAM-3 receptor mediating transient DC–T-cell adhesion required for primary immune response initiation, extending ICAM-3 ligand repertoire beyond integrins.

    Evidence DC-SIGN expression identification, binding assays, anti-DC-SIGN inhibition of DC–T adhesion and proliferation

    PMID:10721994

    Open questions at the time
    • Carbohydrate basis of binding not yet defined at this stage
  11. 2001 High

    Resolved the glycan structures of ICAM-3 and identified the high-mannose component as a candidate DC-SIGN ligand, linking glycosylation to lectin recognition.

    Evidence hydrazinolysis, lectin chromatography, glycosidase digestion, methylation analysis

    PMID:11179968

    Open questions at the time
    • Functional contribution of each glycan species to DC-SIGN binding not directly tested here
  12. 2002 High

    Placed ICAM-3 at the spatiotemporal start of immune-synapse formation, showing it clusters at the T-cell–APC contact-initiation zone before antigen recognition and supports the scanning phase.

    Evidence time-lapse live-cell imaging, antibody blocking of conjugate formation, early signaling and cytoskeletal readouts

    PMID:11812993 PMID:7525599

    Open questions at the time
    • Cytoskeletal adaptors anchoring ICAM-3 at the uropod/contact zone not identified here
  13. 2006 High

    Defined the carbohydrate determinant of DC-SIGN recognition as Lewis-x on myeloid-cell ICAM-3, synthesized primarily by FUT9, refining the glycan-dependent lectin interaction.

    Evidence binding with native ICAM-3, MALDI-TOF glycan identification, FUT isoform cotransfection, Lewis-x mAb staining

    PMID:14970226 PMID:17145745

    Open questions at the time
    • Lymphocyte-derived ICAM-3 binds DC-SIGN by a distinct (mannose) determinant not fully dissected
  14. 2011 High

    Connected ICAM-3 to efferocytosis machinery, showing apoptotic-cell-derived ICAM-3-bearing microparticles act as macrophage chemoattractants and that domain 1–2 tethers dying cells to phagocytes; also identified Kidins220/ARMS as a uropod-associated partner restraining migration.

    Evidence ICAM-3-deficient apoptotic cells, blocking mAbs, chemotaxis/phagocytosis assays, microparticle isolation; co-IP and PKC-regulated colocalization for Kidins220

    PMID:21381019 PMID:22117198

    Open questions at the time
    • Receptor on macrophages capturing microparticle ICAM-3 not fully defined
    • Kidins220–ICAM-3 interaction is single-lab co-IP
  15. 2012 High

    Identified RUNX3 as a negative transcriptional regulator of the leukocyte-restricted ICAM-3 promoter, explaining the downregulation of ICAM-3 during monocyte-to-macrophage differentiation.

    Evidence promoter-reporter assays, ChIP occupancy, RUNX-site mutagenesis, RUNX3 siRNA, differentiation tracking

    PMID:22479382

    Open questions at the time
    • Activating transcription factors driving constitutive leukocyte expression less defined
  16. 2018 Medium

    Extended ICAM-3 function into cancer, defining an intracellular YLPL–Src–AKT axis driving stemness via SOX2/OCT4 and an LFA-1–ICAM-3–ERM mechanical-tension mechanism driving metastasis, building on the earlier AKT–CREB–MMP migration pathway.

    Evidence shRNA knockdown, Src/ERM co-IP with intracellular domain, domain mutants, pathway inhibitors, xenografts, Lifitegrast/LFA-1 blockade; stable OE migration/invasion assays

    PMID:19956847 PMID:29477378 PMID:29729315

    Open questions at the time
    • Single-lab studies for each cancer mechanism
    • YLPL–Src and ERM associations not structurally resolved
    • Direct in vivo clinical relevance unestablished

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the same domain-1 surface and cytoplasmic tail are toggled between LFA-1 adhesion, apoptotic CD14 recognition, and intracellular Src/ERM engagement — and which proteases and conformational switches govern these transitions — remains unresolved.
  • No atomic structure of ICAM-3 in complex with any partner
  • Shedding protease unidentified
  • Mechanism of apoptosis-induced functional switch undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0098631 cell adhesion mediator activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 4
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-1643685 Disease 3
Partners
CD209EZRFYNITGADITGALITGB2KIDINS220LCK

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 ICAM-3 (ICAM-R/CD50) is a member of the immunoglobulin superfamily with five extracellular Ig-like domains that binds LFA-1 (CD11a/CD18), functioning as a third ligand for LFA-1; it is constitutively expressed on all resting leukocytes but not on resting or cytokine-activated endothelial cells. Expression cloning of cDNA, cell adhesion assays, antibody blocking experiments Nature High 1448173 1448174
1992 ICAM-3 (CDw50) becomes phosphorylated on serine residues upon stimulation with protein kinase C activators (phorbol esters, mezerein) and by lymphocyte activation agents (ConA, PHA, anti-CD3 cross-linking); this phosphorylation is rapid, dose-dependent, and inhibited by PKC inhibitors staurosporine and H-7, but does not alter surface expression levels. Radiolabeling with 32P-orthophosphate, phosphoamino acid analysis, PKC inhibitor assays, flow cytometry European journal of biochemistry Medium 1730238
1993 ICAM-3 regulates the LFA-1/ICAM-1 adhesion pathway: engagement of ICAM-3 by activating anti-ICAM-3 mAb (HP2/19, epitope A) triggers LFA-1/ICAM-1-dependent T lymphoblast homotypic aggregation, increases T cell attachment to ICAM-1, and co-stimulates T lymphocyte proliferation with anti-CD3. ICAM-3 localizes to cellular uropods during aggregation, distinct from LFA-1 and ICAM-1 at intercellular boundaries. T cell adhesion assays on purified ICAM-3 surfaces, mAb blocking with anti-LFA-1 and anti-ICAM-1, immunofluorescence microscopy, proliferation assays The Journal of cell biology High 7901223
1993 CDw50 and ICAM-3 are the same glycoprotein (120 kDa surface molecule); identity established by immunochemical, functional, and protein sequencing studies. Protein sequencing, immunochemical cross-reactivity, functional adhesion assays European journal of immunology High 8325327
1994 The LFA-1 binding site on ICAM-3 resides in Ig-like domain 1, which is necessary and sufficient for LFA-1 binding; domain deletion and chimera analysis identified five residues (Asn23, Ser25, Glu37, Phe54, Gln75) that contribute to the binding site, predicted to cluster on the BED face and C/E strands of domain 1 by molecular modeling. Domain deletion mutants, ICAM-3/CD21 chimeras, site-directed mutagenesis (45 point mutants), LFA-1 adhesion assays, epitope mapping with 17 mAbs The Journal of biological chemistry High 8798624
1994 ICAM-3 engagement activates ICAM-3-independent (LFA-1/ICAM-1-independent) cell aggregation in JM T cells and HAFSA B cells; this aggregation involves tyrosine phosphorylation and is regulated by the CD45 tyrosine phosphatase — anti-CD45 mAbs and tyrosine kinase inhibitors abolish ICAM-3-induced aggregation. Tyrosine-phosphorylated proteins (125, 70, 38 kDa) accumulate at intercellular boundaries upon ICAM-3 or LFA-1 engagement. mAb blocking assays, tyrosine kinase inhibitors (herbimycin A), CD45 inhibitors, immunofluorescence, Western blot of phosphotyrosine The Journal of cell biology High 7520448
1994 ICAM-3 engagement by activating mAb (HP2/19) enhances T lymphoblast adhesion to ICAM-1, VCAM-1, fibronectin fragments (FN40, FN80) via increased LFA-1 and VLA-4/VLA-5 avidity, and induces a dramatic uropod-like morphological change with exclusive redistribution of ICAM-3 to the distal uropod tip, while LFA-1 and VLA-β1 remain distributed over the contact area. Cell adhesion assays, mAb blocking, immunofluorescence microscopy, phorbol ester controls The Journal of cell biology High 7525599
1994 Purified ICAM-3 supports LFA-1-dependent T cell adhesion in a temperature- and cation-dependent manner. Combined mAbs to ICAM-1, ICAM-2, and ICAM-3 achieve near-complete inhibition of LFA-1-dependent lymphocyte proliferative responses (PHA, allogeneic cells, specific antigen), suggesting these three molecules account for most or all functional LFA-1 ligands. ICAM-3 also provides a co-stimulatory signal for resting T lymphocyte proliferation. Adhesion assays on purified ICAM-3, mAb blocking of PBL proliferation (PHA, MLR, antigen), T cell co-stimulation assays The Journal of experimental medicine High 7905020
1994 ICAM-3 is a ligand for αdβ2 (CD11d/CD18), a novel fourth β2 integrin that shows preferential binding to ICAM-3 over ICAM-1. cDNA cloning of αd chain, transfection, cell adhesion assays comparing ICAM-3 vs ICAM-1 binding Immunity High 8777714
1994 Cross-linking CD50 (ICAM-3) on Jurkat T cells induces calcium mobilization (primarily via extracellular Ca2+ influx) and tyrosine phosphorylation; p56lck and p59fyn protein tyrosine kinases are found in CD50 immunoprecipitates, implicating these Src-family kinases in CD50 signal transduction. Anti-CD50 cross-linking, intracellular Ca2+ measurement, phosphotyrosine immunoprecipitation, in vitro kinase assays, specific antisera co-immunoprecipitation The Journal of experimental medicine High 7515097
1994 Signaling through CD50 (ICAM-3) increases T lymphocyte adhesion to TNF-stimulated endothelial cells and extracellular matrix proteins by increasing β1 and β2 integrin avidity, without altering surface integrin expression levels. Anti-CD50 mAb stimulation, adhesion to HUVEC and ECM proteins, mAb blocking of β1 and β2 integrins, ICAM-1 transfectant binding, flow cytometry for integrin surface expression European journal of immunology Medium 7515813
1994 The I domain of LFA-1's α subunit contains the binding site for both ICAM-1 and ICAM-3; two I domain mAbs (YTH81.5 and 122.2A5) selectively block ICAM-3 but not ICAM-1 binding, and one I domain mAb (MEM-83) activates binding to ICAM-1 but not ICAM-3, demonstrating that LFA-1 can selectively engage these two highly homologous ligands through the I domain. T cell binding assays to ICAM-1 or ICAM-3-coated plastic, LFA-1 transfected COS cell adhesion assays, mAb epitope mapping to I domain The Journal of cell biology High 7518468
1994 ICAM-3 is a co-stimulatory molecule for both resting and activated T lymphocytes: soluble ICAM-3 or anti-ICAM-3 mAbs co-immobilized with sub-optimal anti-CD3 stimulate CD25 and CD69 expression; this activation is blocked by anti-CD18 mAb, implicating LFA-1 (via its β2 chain) as the mediating integrin. Anti-ICAM-3 (but not anti-ICAM-1) co-stimulates resting cord blood T cells. Co-stimulation assays with immobilized ICAM-3 and anti-CD3, flow cytometry for activation markers (CD25, CD69), mAb blocking with anti-CD18 European journal of immunology Medium 8223855
1994 The LFA-1 binding site in ICAM-3 is in the amino-terminal (domain 1) IgSF domain; electron microscopy shows ICAM-3 is a 15 nm straight rod with head-to-tail domain arrangement; residues E37/T38 form a conserved integrin binding site motif also found in ICAM-1 and VCAM-1, while Q75 may confer LFA-1 binding specificity. Electron microscopy, domain deletion mutants, site-directed mutagenesis, mAb blocking adhesion assays Cell adhesion and communication High 7531103
1994 ICAM-3 surface expression on activated neutrophils is rapidly downregulated by a proteolytic shedding mechanism (not internalization): protease inhibitors block PMA-induced downregulation, and ICAM-3 is detected in cell-free supernatants and in plasma (0-296 ng/ml). The remaining ICAM-3 on the neutrophil surface still supports anti-ICAM-3-triggered homotypic aggregation. Immunofluorescence flow cytometry, 125I-labeled mAb internalization assay, immunoprecipitation of supernatants, radioimmunoassay of plasma, protease inhibitor studies European journal of immunology High 7525295
1994 ICAM-3 is not a ligand for Mac-1 (CD11b/CD18) or p150,95 (CD11c/CD18): purified ICAM-3 from lymphoid cells and neutrophils does not support adhesion of Mac-1- or p150,95-expressing CHO transfectants, and purified Mac-1 does not support adhesion of ICAM-3-expressing L cell transfectants, despite ICAM-3 being well expressed on neutrophils where Mac-1 is abundant. Cell adhesion assays with CHO and L cell transfectants expressing specific integrins, homotypic aggregation assays European journal of immunology High 7737271
1995 CD50 (ICAM-3) is phosphorylated on tyrosine in human neutrophils (predominantly phosphotyrosine by phosphoamino acid analysis); phosphorylation increases transiently (peak ~1 min) after stimulation with FMLP, PAF, PMA, or calcium ionophore. Tyrosine kinase activity is detected in CD50 immunoprecipitates from solubilized neutrophils. Radiolabeling ecto-kinase assay, phosphoamino acid analysis, immunoprecipitation in vitro kinase assay Journal of immunology Medium 7876557
1995 A circulating/soluble form of ICAM-3 (sCD50) is produced by lymphocytes upon activation (particularly CD3 triggering), is proteolytically cleaved from the cell membrane (apparent MW ~95 kDa vs membrane ~120 kDa by immunoblot), and is detectable in normal human serum; sCD50 levels are elevated in SLE patients and correlate positively with sCD27 levels. Sandwich ELISA, immunoblot of culture supernatants, Northern blot kinetics, flow cytometry for surface expression Journal of immunology Medium 7876564
1996 Stimulation through CD50 (ICAM-3) on human thymocytes by mAb cross-linking induces calcium mobilization and CD69 (but not CD25) expression; co-cross-linking with CD45 inhibits calcium mobilization, implicating tyrosine phosphorylation in CD50 signaling. CD50 cross-linking also increases activation-induced cell death of thymocytes. mAb cross-linking, intracellular Ca2+ measurement, co-cross-linking with anti-CD45, flow cytometry for activation markers, apoptosis assays Tissue antigens Medium 9008304
1997 The LFA-1 I domain alone (expressed as GPI-anchored) is sufficient to mediate transient, Mg2+-dependent rolling adhesion on ICAM-1 and ICAM-3 in hydrodynamic flow. MEM-83 (activating I domain mAb) decreased rolling velocity on ICAM-1 but blocked rolling on ICAM-3, demonstrating that ICAM-3 interaction with the I domain is blocked by this conformational change. Stable GPI-anchored I domain expression, flow cell rolling assays on lipid bilayers with purified ICAM-1 or ICAM-3, activating mAb (MEM-83) treatment, divalent cation substitution The Journal of experimental medicine High 9271587
1998 The LFA-1 binding site on ICAM-3 domain 1 is more extensive than that of ICAM-1, involving residues on both the ABED face and GFC face; point mutagenesis of 18 residues identified 7 that reduce or abolish LFA-1 adhesion, including 3 on the A strand of the ABED face — a surface not used by ICAM-1 for LFA-1 binding. 18-point mutagenesis of domain 1, LFA-1 adhesion assays, functional blocking mAb binding studies Journal of immunology High 9686599
1998 ICAM-3 engagement on monocytes and neutrophils by domain 1-directed triggering mAbs induces outside-in signaling: monocytes secrete chemokines MIP-1α, IL-8, and MCP-1; neutrophils secrete IL-8; monocytes show dramatic spreading via Fab/F(ab')2 fragments (excluding Fc-mediated effects). Co-engagement of ICAM-3 and Fc receptors (FcγRI or FcγRII) is required for maximal chemokine secretion by monocytes. Immobilized mAb engagement, ELISA for chemokines, Fab/F(ab')2 fragment controls, microscopy of cell spreading Journal of immunology High 9605163
1998 ICAM-3 engagement on PMN (by CAL3.10 mAb binding in the αLβ2 integrin-binding region) activates PMN homotypic aggregation and adhesion via outside-in signaling: β2 integrin-dependent mechanism, activates tyrosine and PKC kinases, and reorganizes the cytoskeleton without causing degranulation or increasing surface β2 integrin expression. A different anti-ICAM-3 mAb (HP2/19) does not activate PMN, demonstrating epitope-specificity. PMN aggregation assays, F(ab')2 fragment controls, anti-β2 integrin blocking, kinase activity assays, cytoskeleton reorganization assays, degranulation assays (elastase release), flow cytometry for β2 integrin expression Journal of immunology High 9834117
1999 ICAM-3 on the surface of apoptotic leukocytes acquires altered receptor-binding activity: during apoptosis, the first Ig-like domain of ICAM-3 participates in macrophage recognition and phagocytosis of apoptotic cells. ICAM-3 on apoptotic cells switches binding preference from LFA-1 to an alternative macrophage receptor; mAb blockade of macrophage CD14 (but not αvβ3 or αdβ2) inhibited ICAM-3-dependent recognition of apoptotic cells. mAb blocking of macrophage-apoptotic cell interactions, ICAM-3 transfection into non-leukocytes, multiple apoptosis stimuli, domain 1-specific mAb characterization Journal of immunology High 10352301
2000 DC-SIGN, a novel dendritic cell-specific C-type lectin, binds ICAM-3 expressed on resting T cells with high affinity and mediates transient DC-T cell adhesion required for initiation of primary immune responses; antibodies against DC-SIGN inhibit DC-induced proliferation of resting T cells. Identification of DC-SIGN by expression, binding assays, anti-DC-SIGN mAb inhibition of DC-T cell adhesion and T cell proliferation Cell High 10721994
2000 LFA-1 binding to ICAM-3 (vs ICAM-1 or ICAM-2) produces distinct cytokine profiles in T cells: ICAM-2 and ICAM-3 co-stimulation induces stronger TNF-α secretion, whereas ICAM-1 co-stimulation induces higher IL-10 production, demonstrating that the specific ICAM ligand engaged by LFA-1 differentially shapes the Th1/Th2 cytokine output. T cell co-stimulation assays on immobilized ICAM-1, -2, or -3, cytokine ELISA (GM-CSF, IFN-γ, IL-2, IL-4, IL-5, IL-10, TNF-α), proliferation assays European journal of immunology Medium 10427988
2000 LFA-1 binds ICAM-3 as its primary ligand supporting neutrophil homotypic adhesion at high shear rates (≥800 s-1), while Mac-1 predominates at low shear rates (~100 s-1); ICAM-3 supports LFA-1-mediated homotypic neutrophil aggregation with efficiency varying with shear rate and time post-stimulation. Cone-plate viscometer shear assay, flow cytometry aggregate quantification, mAb blocking of LFA-1, Mac-1, and ICAM-3, collision efficiency modeling Journal of immunology Medium 10725740
2001 ICAM-3 N-linked oligosaccharides are predominantly tri- and tetra-antennary complex-type (~6 mol/mol protein) with poly-N-acetyllactosamine chains; a small amount of high-mannose oligosaccharide (6 α-mannose residues) is present, which can serve as a ligand for DC-SIGN. Hydrazinolysis, paper electrophoresis, lectin column chromatography, sequential glycosidase digestion, methylation analysis, structural characterization European journal of biochemistry High 11179968
2002 ICAM-3 is specifically clustered at the region of the T lymphocyte surface that initiates contact with APCs before antigen recognition (as shown by time-lapse live imaging), and plays a role in T cell-APC conjugate formation, early intracellular signaling, and cytoskeletal rearrangement in the initial APC-scanning phase. Time-lapse live-cell imaging, antibody blocking of T cell-APC conjugate formation, early signaling assays, cytoskeletal rearrangement assays Nature immunology High 11812993
2004 DC-SIGN binds to gp120 in a distinct but overlapping manner compared to ICAM-2 and ICAM-3: recombinant soluble DC-SIGN binds gp120 >100-fold and >50-fold better than ICAM-2-Fc and ICAM-3-Fc, respectively; Asp-367 mutation enhances gp120 binding but diminishes ICAM-2 and ICAM-3 binding, while Gly-346 mutation abrogates gp120 binding but enhances ICAM-2/ICAM-3 binding. Recombinant protein binding assays (ICAM-2-Fc, ICAM-3-Fc, gp120-Fc), alanine-scanning mutagenesis of DC-SIGN, monosaccharide/disaccharide competition, glycan chip analysis The Journal of biological chemistry High 14970226
2006 DC-SIGN binds native ICAM-3 isolated from peripheral leukocytes via Lewis x (Lex) carbohydrate residues; ICAM-3 from granulocytes (not lymphocytes) bears Lex residues mediating DC-SIGN binding; FUT IX is the primary fucosyltransferase mediating Lex synthesis on ICAM-3 in myeloid cells, with minor contribution from FUT IV. DC-SIGN binding assays with native ICAM-3, Lewis x mAb staining, MALDI-TOF mass spectrometry for Lex confirmation, cotransfection of FUT isoforms (FUT III, IV, VII, IX) with ICAM-3, flow cytometry Glycobiology High 17145745
2011 Apoptotic cell-derived microparticles bearing ICAM-3 potently attract macrophages (chemoattraction) to sites of leukocyte cell death; ICAM-3 on apoptotic cells mediates domain 1-2-dependent tethering to phagocytes. Apoptosis causes reduction in cell-surface ICAM-3 via release within microparticles. Blocking mAb (MA4) that inhibits domain 1-2 of ICAM-3 blocks apoptotic cell clearance. Novel anti-ICAM-3 mAb blocking studies, ICAM-3-deficient apoptotic leukocytes, macrophage chemotaxis assays, microparticle isolation and characterization, phagocytosis assays Cell death and differentiation High 22117198
2012 ICAM-3 gene promoter activity is leukocyte-restricted and is negatively regulated by RUNX transcription factors: RUNX cognate sequences are required for promoter activity and RUNX3/Ets/C-EBP cooperative regulation; siRNA-mediated reduction of RUNX3 increases ICAM-3 mRNA levels. ICAM-3 protein levels decrease during monocyte-to-macrophage differentiation and monocyte transendothelial migration, correlating with RUNX3 increase. ICAM-3 promoter-reporter assays, chromatin immunoprecipitation (in vivo occupancy), RUNX-binding site mutagenesis, siRNA knockdown of RUNX3, protein analysis during differentiation/migration PloS one High 22479382
2013 ICAM-3 expressed on macrophages functions as a recognition receptor for apoptotic neutrophils: siRNA silencing and antibody blockade of ICAM-3 on macrophages (but not neutrophils) reduces phagocytosis; blocking ICAM-3 on apoptotic neutrophil surface also reduces uptake. ICAM-3 and LFA-1 (αL/β2) co-localize at phagocytic portals on macrophages; simultaneous knockdown causes marked phagocytosis deficiency. Gene silencing (siRNA), blocking antibodies, confocal microscopy of phagocytic portals, apoptotic neutrophil phagocytosis assay Apoptosis High 23775590
2010 ICAM-3 overexpression in NSCLC cells increases cell migration and invasion by upregulating MMP-2 and MMP-9 expression and activity through a signaling pathway: ICAM-3 → Akt phosphorylation → CREB activation → MMP upregulation. Blocking the Akt pathway attenuates CREB activation and reduces MMP activity and migration/invasion, regardless of p53 or PTEN status. Stable ICAM-3-overexpressing transfectants, migration/invasion assays, MMP-2/9 activity assays, Akt phosphorylation Western blot, CREB activation assays, Akt pathway inhibitors, CREB siRNA International journal of oncology Medium 19956847
2018 ICAM-3 promotes cancer cell stemness by recruiting and binding Src kinase via a YLPL motif in its intracellular domain, thereby activating PI3K-AKT signaling that enhances SOX2 and OCT4 activity; activated p-AKT also facilitates p50 nuclear translocation enhancing ICAM-3 promoter activity creating a positive feedback loop. ICAM-3 knockdown reduces side population, sphere formation, chemo-resistance, and tumor growth in vivo. siRNA screen, shRNA knockdown, Src co-immunoprecipitation with intracellular domain, Src/PI3K inhibitors, in vivo tumor xenograft, ALDH assay, sphere formation, p50 nuclear translocation assay, ICAM-3 promoter ChIP Cancer letters Medium 29477378
2018 ICAM-3 promotes tumor metastasis through a LFA-1-ICAM-3-ERM-lamellipodia mechanism: ICAM-3 binds LFA-1 via its extracellular domain and ERM proteins via its intracellular domain, creating mechanical tension that facilitates cell separation (metastasis). ICAM-3 extracellular or intracellular domain mutants abolish ICAM-3-mediated metastasis in vitro and in vivo; blocking LFA-1/ICAM-3 interaction with LFA-1 antibody or Lifitegrast reduces metastasis. Co-IP of LFA-1 and ERM with ICAM-3, extracellular/intracellular domain mutants, in vitro and in vivo metastasis assays, LFA-1 blocking antibody and Lifitegrast treatment Biochimica et biophysica acta. Molecular basis of disease Medium 29729315
2011 Kidins220/ARMS (a neuronal scaffold protein also expressed in T cells) co-localizes with and co-immunoprecipitates with ICAM-3 at the uropod of polarized T cells; this association requires cell polarity and is regulated by PKC. Kidins220/ARMS knockdown promotes basal and SDF-1α-induced T cell directed migration. Co-immunoprecipitation, confocal immunofluorescence colocalization, cell polarity disruption, PKC inhibition, siRNA knockdown, chemotaxis assays European journal of immunology Medium 21381019
2004 Activation of ICAM-3 on human bone marrow endothelial cells by antibody cross-linking reduces electrical resistance of endothelial monolayers and causes loss of cell-cell contacts; cross-linking induces association of moesin (and later ezrin) with ICAM-3, and stimulates production of reactive oxygen species (ROS) that mediate control of endothelial integrity. Electrical resistance measurements, immunocytochemistry, biochemical pull-down/co-IP of moesin and ezrin, ROS detection Journal of vascular research Medium 14726630

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Identification of DC-SIGN, a novel dendritic cell-specific ICAM-3 receptor that supports primary immune responses. Cell 1340 10721994
2003 Dendritic-cell-specific ICAM3-grabbing non-integrin is essential for the productive infection of human dendritic cells by mosquito-cell-derived dengue viruses. EMBO reports 383 12783086
1992 Molecular cloning of ICAM-3, a third ligand for LFA-1, constitutively expressed on resting leukocytes. Nature 322 1448173
1995 A novel leukointegrin, alpha d beta 2, binds preferentially to ICAM-3. Immunity 224 8777714
1992 Cloning and characterization of a new intercellular adhesion molecule ICAM-R. Nature 198 1448174
1994 Characterization of the function of intercellular adhesion molecule (ICAM)-3 and comparison with ICAM-1 and ICAM-2 in immune responses. The Journal of experimental medicine 156 7905020
1993 ICAM-3 interacts with LFA-1 and regulates the LFA-1/ICAM-1 cell adhesion pathway. The Journal of cell biology 150 7901223
1994 Differential distribution of intercellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) and the MS-1 antigen in normal and diseased human synovia. Their possible pathogenetic and clinical significance in rheumatoid arthritis. Arthritis and rheumatism 133 8129777
1999 Macrophage recognition of ICAM-3 on apoptotic leukocytes. Journal of immunology (Baltimore, Md. : 1950) 125 10352301
2002 Role of ICAM-3 in the initial interaction of T lymphocytes and APCs. Nature immunology 123 11812993
1995 The increased expression of adhesion molecules ICAM-3, E- and P-selectins on breast cancer endothelium. The Journal of pathology 119 8568591
2002 Functional evaluation of DC-SIGN monoclonal antibodies reveals DC-SIGN interactions with ICAM-3 do not promote human immunodeficiency virus type 1 transmission. Journal of virology 103 12021323
1994 Induction of tyrosine phosphorylation during ICAM-3 and LFA-1-mediated intercellular adhesion, and its regulation by the CD45 tyrosine phosphatase. The Journal of cell biology 98 7520448
2010 Human neutrophils interact with both 6-sulfo LacNAc+ DC and NK cells to amplify NK-derived IFN{gamma}: role of CD18, ICAM-1, and ICAM-3. Blood 89 21098395
2011 Apoptotic cell-derived ICAM-3 promotes both macrophage chemoattraction to and tethering of apoptotic cells. Cell death and differentiation 88 22117198
1993 ICAM-3, the third LFA-1 counterreceptor, is a co-stimulatory molecule for both resting and activated T lymphocytes. European journal of immunology 88 8223855
2009 Human milk oligosaccharides reduce HIV-1-gp120 binding to dendritic cell-specific ICAM3-grabbing non-integrin (DC-SIGN). The British journal of nutrition 86 19230080
2006 The location of asparagine-linked glycans on West Nile virions controls their interactions with CD209 (dendritic cell-specific ICAM-3 grabbing nonintegrin). The Journal of biological chemistry 85 17001080
1994 Involvement of the "I" domain of LFA-1 in selective binding to ligands ICAM-1 and ICAM-3. The Journal of cell biology 82 7518468
2004 Dynamic populations of dendritic cell-specific ICAM-3 grabbing nonintegrin-positive immature dendritic cells and liver/lymph node-specific ICAM-3 grabbing nonintegrin-positive endothelial cells in the outer zones of the paracortex of human lymph nodes. The American journal of pathology 78 15111305
2010 ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB. International journal of oncology 75 19956847
2000 Changed colonic profile of P-selectin, platelet-endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), ICAM-2, and ICAM-3 in inflammatory bowel disease. Clinical and experimental immunology 75 10931137
1994 ICAM-3 regulates lymphocyte morphology and integrin-mediated T cell interaction with endothelial cell and extracellular matrix ligands. The Journal of cell biology 73 7525599
2010 Functional interaction of common allergens and a C-type lectin receptor, dendritic cell-specific ICAM3-grabbing non-integrin (DC-SIGN), on human dendritic cells. The Journal of biological chemistry 72 20080962
1994 CD50 (intercellular adhesion molecule 3) stimulation induces calcium mobilization and tyrosine phosphorylation through p59fyn and p56lck in Jurkat T cell line. The Journal of experimental medicine 65 7515097
2005 Specific ICAM-3 grabbing nonintegrin-related 1 (SIGNR1) expressed by marginal zone macrophages is essential for defense against pulmonary Streptococcus pneumoniae infection. European journal of immunology 61 16134084
1997 The lymphocyte function-associated antigen 1 I domain is a transient binding module for intercellular adhesion molecule (ICAM)-1 and ICAM-3 in hydrodynamic flow. The Journal of experimental medicine 57 9271587
1997 RANTES stimulation of T lymphocyte adhesion and activation: role for LFA-1 and ICAM-3. European journal of immunology 54 9174593
1994 Signaling through CD50 (ICAM-3) stimulates T lymphocyte binding to human umbilical vein endothelial cells and extracellular matrix proteins via an increase in beta 1 and beta 2 integrin function. European journal of immunology 54 7515813
1995 Adhesion molecules intercellular adhesion molecule-1 (ICAM-1), ICAM-3 and B7 are not expressed by epithelium in normal or inflamed colon. Clinical and experimental immunology 53 7542573
2011 Retagging identifies dendritic cell-specific intercellular adhesion molecule-3 (ICAM3)-grabbing non-integrin (DC-SIGN) protein as a novel receptor for a major allergen from house dust mite. The Journal of biological chemistry 50 22205703
2004 DC-SIGN binds to HIV-1 glycoprotein 120 in a distinct but overlapping fashion compared with ICAM-2 and ICAM-3. The Journal of biological chemistry 50 14970226
1994 Expression of ICAM-R (ICAM-3), a novel counter-receptor for LFA-1, in rheumatoid and nonrheumatoid synovium. Comparison with other adhesion molecules. Arthritis and rheumatism 45 7516162
1995 Circulating forms of ICAM-3 (cICAM-3). Elevated levels in autoimmune diseases and lack of association with cICAM-1. Journal of immunology (Baltimore, Md. : 1950) 44 7836774
1994 Intercellular adhesion molecules (ICAM)-1 ICAM-2 and ICAM-3 function as counter-receptors for lymphocyte function-associated molecule 1 in human immunodeficiency virus-mediated syncytia formation. European journal of immunology 44 7916296
1999 Human T-cell leukaemia/lymphoma virus type 1 syncytium formation is regulated in a cell-specific manner by ICAM-1, ICAM-3 and VCAM-1 and can be inhibited by antibodies to integrin beta2 or beta7. The Journal of general virology 43 10374960
1999 Co-stimulation of T cells results in distinct IL-10 and TNF-alpha cytokine profiles dependent on binding to ICAM-1, ICAM-2 or ICAM-3. European journal of immunology 43 10427988
2000 Shear and time-dependent changes in Mac-1, LFA-1, and ICAM-3 binding regulate neutrophil homotypic adhesion. Journal of immunology (Baltimore, Md. : 1950) 42 10725740
1996 Localization of the binding site on intercellular adhesion molecule-3 (ICAM-3) for lymphocyte function-associated antigen 1 (LFA-1). The Journal of biological chemistry 41 8798624
1994 Regulation of ICAM-3 (CD50) membrane expression on human neutrophils through a proteolytic shedding mechanism. European journal of immunology 40 7525295
1993 CDw50 and ICAM-3: two names for the same molecule. European journal of immunology 40 8325327
2018 ICAM3 mediates inflammatory signaling to promote cancer cell stemness. Cancer letters 37 29477378
2013 Novel role of ICAM3 and LFA-1 in the clearance of apoptotic neutrophils by human macrophages. Apoptosis : an international journal on programmed cell death 37 23775590
2007 Investigation of promoter variations in dendritic cell-specific ICAM3-grabbing non-integrin (DC-SIGN) (CD209) and their relevance for human cytomegalovirus reactivation and disease after allogeneic stem-cell transplantation. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases 37 18076668
2005 The changes in expression of ICAM-3, Ki-67, PCNA, and CD31 in psoriatic lesions before and after methotrexate treatment. Archives of dermatological research 37 16215763
1995 CD50 (ICAM-3) is phosphorylated on tyrosine and is associated with tyrosine kinase activity in human neutrophils. Journal of immunology (Baltimore, Md. : 1950) 35 7876557
2007 Structural requirements for multimerization of the pathogen receptor dendritic cell-specific ICAM3-grabbing non-integrin (CD209) on the cell surface. The Journal of biological chemistry 34 18073208
2005 Increased expression of ICAM-3 is associated with radiation resistance in cervical cancer. International journal of cancer 32 15880373
2012 RUNX3 regulates intercellular adhesion molecule 3 (ICAM-3) expression during macrophage differentiation and monocyte extravasation. PloS one 31 22479382
1994 Cellular distribution of human leucocyte adhesion molecule ICAM-3. Journal of clinical pathology 31 8132828
2002 Binding of LFA-1 (CD11a) to intercellular adhesion molecule 3 (ICAM-3; CD50) and ICAM-2 (CD102) triggers transmigration of human immunodeficiency virus type 1-infected monocytes through mucosal epithelial cells. Journal of virology 30 11739669
1994 LFA-1 binding site in ICAM-3 contains a conserved motif and non-contiguous amino acids. Cell adhesion and communication 30 7531103
1993 ICAM-3 expression on endothelium in lymphoid malignancy. The American journal of pathology 30 8214000
2008 Cooperation of specific ICAM-3 grabbing nonintegrin-related 1 (SIGNR1) and complement receptor type 3 (CR3) in the uptake of oligomannose-coated liposomes by macrophages. Glycobiology 29 19029201
1995 Epitope mapping and functional properties of anti-intercellular adhesion molecule-3 (CD50) monoclonal antibodies. European journal of immunology 29 7875209
1995 Existence of a soluble form of CD50 (intercellular adhesion molecule-3) produced upon human lymphocyte activation. Present in normal human serum and levels are increased in the serum of systemic lupus erythematosus patients. Journal of immunology (Baltimore, Md. : 1950) 29 7876564
2007 Association of ICAM3 genetic variant with severe acute respiratory syndrome. The Journal of infectious diseases 28 17570115
2006 DC-SIGN binds ICAM-3 isolated from peripheral human leukocytes through Lewis x residues. Glycobiology 28 17145745
1995 Heterogenous glycosylation of ICAM-3 and lack of interaction with Mac-1 and p150,95. European journal of immunology 27 7737271
2017 Increased Cell Adhesion Molecules, PECAM-1, ICAM-3, or VCAM-1, Predict Increased Risk for Flare in Patients With Quiescent Inflammatory Bowel Disease. Journal of clinical gastroenterology 26 27552332
1998 Coengagement of ICAM-3 and Fc receptors induces chemokine secretion and spreading by myeloid leukocytes. Journal of immunology (Baltimore, Md. : 1950) 24 9605163
1999 ICAM-3 and E-selectin endothelial cell expression differentiate two phases of angiogenesis in infantile hemangiomas. Journal of cutaneous pathology 23 10189240
1998 Induction of sensitivity to NK-mediated cytotoxicity by TNF-alpha treatment: possible role of ICAM-3 and CD44. Leukemia 23 9766501
2018 ICAM3 mediates tumor metastasis via a LFA-1-ICAM3-ERM dependent manner. Biochimica et biophysica acta. Molecular basis of disease 22 29729315
2001 Structural study of N-linked oligosaccharides of human intercellular adhesion molecule-3 (CD50). European journal of biochemistry 22 11179968
2008 Binding of the Streptococcus gordonii DL1 surface protein Hsa to the host cell membrane glycoproteins CD11b, CD43, and CD50. Infection and immunity 21 18678668
1997 Antibodies to the beta 1-integrin chain, CD44, or ICAM-3 stimulate adhesion of blast colony-forming cells and may inhibit their growth. Experimental hematology 21 9131010
2018 Targeting Mycobacterium tuberculosis Antigens to Dendritic Cells via the DC-Specific-ICAM3-Grabbing-Nonintegrin Receptor Induces Strong T-Helper 1 Immune Responses. Frontiers in immunology 19 29662482
2000 Human leukemic (HMC-1) mast cells are responsive to 1alpha, 25-dihydroxyvitamin D(3): selective promotion of ICAM-3 expression and constitutive presence of vitamin D(3) receptor. Biochemical and biophysical research communications 19 10891379
1995 B-cell homotypic adhesion through exon-A restricted epitopes of CD45 involves LFA-1/ICAM-1, ICAM-3 interactions, and induces coclustering of CD45 and LFA-1. Blood 19 7544645
2004 ICAM-3 activation modulates cell-cell contacts of human bone marrow endothelial cells. Journal of vascular research 18 14726630
1994 The human intercellular adhesion molecule 3 (ICAM3) gene is located in the 19p13.2-p13.3 region, close to the ICAM1 gene. Genomics 18 7851905
1999 Regulation of ICAM-3 and other adhesion molecule expressions on eosinophils in vitro. Effects of dexamethasone. Allergy 17 10688433
2001 Retinoic acid up-regulates myeloid ICAM-3 expression and function in a cell-specific fashion--evidence for retinoid signaling pathways in the mast cell lineage. Journal of leukocyte biology 15 11261782
1998 Engagement of ICAM-3 activates polymorphonuclear leukocytes: aggregation without degranulation or beta 2 integrin recruitment. Journal of immunology (Baltimore, Md. : 1950) 15 9834117
1995 Intercellular adhesion molecule-3 (CD50) on human epidermal Langerhans cells participates in T-cell activation. The Journal of investigative dermatology 15 7539471
2000 CD4+ T cell and eosinophil adhesion is mediated by specific ICAM-3 ligation and results in eosinophil activation. Journal of immunology (Baltimore, Md. : 1950) 14 10706734
1998 Mapping of the ICAM-5 (telencephalin) gene, a neuronal member of the ICAM family, to a location between ICAM-1 and ICAM-3 on human chromosome 19p13.2. Genomics 14 9828136
1997 CD50 monoclonal antibodies inhibit neutrophil activation. Journal of immunology (Baltimore, Md. : 1950) 14 9218600
1996 Stimulation through CD50 (ICAM-3) induces both activation and programmed cell death of human thymocytes. Tissue antigens 14 9008304
1995 CD50 (intercellular adhesion molecule-3) is expressed at higher levels on memory than on naive human T cells but induces a similar calcium mobilization on both subsets. Tissue antigens 14 7482494
2013 ICAM-3 endows anticancer drug resistance against microtubule-damaging agents via activation of the ICAM-3-AKT/ERK-CREB-2 pathway and blockage of apoptosis. Biochemical and biophysical research communications 13 24177012
2011 The neuronal protein Kidins220/ARMS associates with ICAM-3 and other uropod components and regulates T-cell motility. European journal of immunology 13 21381019
2000 Soluble and cell surface ICAM-3 in blood and cerebrospinal fluid of patients with multiple sclerosis: influence of methylprednisolone treatment and relevance as markers for disease activity. Acta neurologica Scandinavica 13 10685862
1998 The leukocyte function-associated antigen-1 (LFA-1)-binding site on ICAM-3 comprises residues on both faces of the first immunoglobulin domain. Journal of immunology (Baltimore, Md. : 1950) 13 9686599
1992 Effect of protein kinase C activators on the phosphorylation and the surface expression of the CDw50 leukocyte antigen. European journal of biochemistry 13 1730238
2000 CD50 and CD62L adhesion receptor expression on naive (CD45RA+) and memory (CD45RO+) T lymphocytes in the elderly. Pathobiology : journal of immunopathology, molecular and cellular biology 12 11493756
2000 CD45RA+ ICAM-3+ lymphocytes in cerebrospinal fluid and blood as markers of disease activity in patients with multiple sclerosis. Acta neurologica Scandinavica 11 11083511
1999 ICAM-3 (CD50) cross-linking augments signaling in CD3-activated peripheral human T lymphocytes. Journal of leukocyte biology 10 10380912
1995 Expression of ICAM-3/CD50 in normal and diseased skin. The British journal of dermatology 10 8546991
1996 Expression of intercellular adhesion molecule-3 (ICAM-3/CD50) in malignant lymphoproliferative disorders and solid tumors. Tissue antigens 9 8946680
2019 ICAM3-Fc Outperforms Receptor-Specific Antibodies Targeted Nanoparticles to Dendritic Cells for Cross-Presentation. Molecules (Basel, Switzerland) 8 31083610
1995 Expression of ICAM-3 on human epidermal dendritic cells. Immunobiology 8 7782098
1993 Isolation and characterisation of a CDw50 negative Jurkat T-cell line variant (PPL.1). Leukemia research 8 8429685
2007 ICAM-3 influences human immunodeficiency virus type 1 replication in CD4(+) T cells independent of DC-SIGN-mediated transmission. Virology 7 17434553
1999 ICAM-3 (CD50) is expressed by human mast cells: induction of homotypic mast cell aggregation via ICAM-3. Cell adhesion and communication 7 10626904
1998 Stimulation through CD50 preferentially induces apoptosis of TCR1+ human peripheral blood lymphocytes. Cell adhesion and communication 7 9929740
2007 An intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) efficiently blocks HIV viral budding. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 6 17962491
2005 ICAM-3, a ligand for DC-SIGN, was duplicated from ICAM-1 in mammalian evolution, but was lost in the rodent genome. FEBS letters 6 15890347
1995 Expression of the intercellular adhesion molecule-3 (ICAM-3) in human renal tissue with relation to kidney transplants and various inflammatory diseases. APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 6 7576578

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