Affinage

Showing CD226 — PTA1 is a alias.

CD226

CD226 antigen · UniProt Q15762

Length
336 aa
Mass
38.6 kDa
Annotated
2026-06-09
100 papers in source corpus 38 papers cited in narrative 38 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD226 (DNAM-1) is an immunoglobulin-superfamily transmembrane glycoprotein with two V-set domains that functions as an activating adhesion and signaling receptor central to cytotoxic lymphocyte function and immunosurveillance (PMID:8673704, PMID:9268302). It engages the nectin-family ligands CD155 (PVR) and CD112 (Nectin-2) through a side-by-side tandem D1–D2 IgV arrangement, in which D1 forms the conserved interface with CD155 while D2 provides structural support and direct contacts required for high-affinity binding (PMID:15039383, PMID:30591568). Ligand engagement triggers Src-family kinase-mediated tyrosine phosphorylation of a cytoplasmic ITT-like motif (residue Y322/Y319 critical for adhesive and signaling function) that recruits Grb2 and activates Vav-1, PI3K, PLCγ1, Erk, and Akt, driving actin polymerization, granule polarization, calcium flux, cytokine production, and phosphorylation-mediated inactivation of FOXO1 (PMID:12847109, PMID:26552706, PMID:30504141). Serine phosphorylation at S329 instead promotes physical association with LFA-1, which carries CD226 into lipid rafts at the immunological synapse; this LFA-1 partnership is required for CD226 tyrosine phosphorylation and costimulatory signaling, and Fyn mediates the bidirectional phosphorylation between the two receptors (PMID:10591186, PMID:14676297, PMID:15684041, PMID:16636013). CD226 competes with the inhibitory receptor TIGIT (and outcompetes CD96) for the shared CD155 ligand, and the CD226/TIGIT balance dictates effector versus regulatory outcomes in CD8+ T cells, NK cells, and Tregs (PMID:22427644, PMID:32040157, PMID:34011606). Through these mechanisms CD226 is required in vivo for tumor immunosurveillance across transplant, carcinogen-induced, and myeloma models, for NK- and monocyte-dependent control of cytomegalovirus, and for diverse inflammatory functions including monocyte transendothelial migration, macrophage polarization, Treg stability in autoimmunity, and ILC2-dependent airway hyperreactivity (PMID:15136589, PMID:19029379, PMID:25893601, PMID:37625150, PMID:38244725, PMID:27503073). Receptor abundance is itself regulated: tumor-derived CD155 drives Y319 phosphorylation enabling CBL-B-mediated ubiquitination and proteasomal degradation, and Eomes transcriptionally represses CD226 in CD8+ T cells, with loss of CD226 producing checkpoint-blockade-resistant exhausted T cells (PMID:33053330, PMID:33053331).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1985 Medium

    Before its molecular identity was known, antibody blockade established that this T-lineage activation antigen is functionally required for the differentiation of cytotoxic effectors from precursors.

    Evidence mAb/F(ab')2 blockade in mixed lymphocyte culture with limiting dilution analysis

    PMID:2580933

    Open questions at the time
    • Molecular identity of TLiSA1 not yet established
    • No receptor signaling or ligand defined
  2. 1989 Medium

    Linked CD226 surface expression to an upstream regulatory cue by showing TGF-β suppresses it in parallel with cytotoxic effector differentiation.

    Evidence Mixed lymphocyte culture with TGF-β treatment, mAb blockade, and anti-TGF-β rescue

    PMID:2541074

    Open questions at the time
    • Mechanism of TGF-β transcriptional control unknown
    • No molecular cloning yet
  3. 1996 High

    Defined CD226 as a tyrosine-phosphorylated signal-transducing adhesion molecule required for CTL and NK cytotoxicity, establishing it as more than a passive adhesion antigen.

    Evidence mAb blocking, immunoprecipitation, and cytotoxicity assays

    PMID:8673704

    Open questions at the time
    • Ligand not identified
    • Specific phosphosites and downstream effectors unknown
  4. 1997 High

    Molecular cloning unified the T-cell antigen TLiSA1 and platelet antigen PTA1 as a single two-IgV-domain immunoglobulin superfamily protein, resolving its identity and domain architecture.

    Evidence cDNA cloning, peptide sequencing, RT-PCR, flow cytometry, pharmacological perturbation

    PMID:9268302

    Open questions at the time
    • Ligand and signaling partners still unknown
    • Cytoplasmic motif function uncharacterized
  5. 1999 High

    Established the functional partnership with LFA-1, showing serine phosphorylation drives the association and Fyn mediates LFA-1-induced CD226 tyrosine phosphorylation, with genetic rescue in LAD NK cells.

    Evidence Reciprocal co-IP, genetic reconstitution of LFA-1 in LAD patient NK cells, phosphorylation assays

    PMID:10591186

    Open questions at the time
    • Precise serine residue not yet mapped
    • Downstream signaling cascade undefined
  6. 2003 High

    Mapped the critical Y322 residue for adhesive and costimulatory function across platelet adhesion and naive T cell costimulation, and localized the LFA-1/CD226/Fyn complex to the immunological synapse.

    Evidence Y322F site-directed mutagenesis, lentiviral transduction, adhesion and T cell proliferation/Th1 differentiation assays, synapse imaging

    PMID:12847109 PMID:14676297

    Open questions at the time
    • Adaptor recruited by phospho-Y322 not yet identified
    • Distinction between adhesion and signaling functions incomplete
  7. 2004 High

    Identified CD155 (PVR) and CD112 (Nectin-2) as the activating ligands and demonstrated cooperation with LFA-1 in triggering cytotoxicity, and showed CD226-PVR governs the diapedesis step of monocyte transendothelial migration.

    Evidence Ectopic ligand expression, cytotoxicity and mAb blocking, soluble DNAM-1-Fc binding, transmigration assays with confocal microscopy

    PMID:15039383 PMID:15136589

    Open questions at the time
    • Relative ligand affinities not quantified
    • Structural basis of binding unknown
  8. 2005 High

    Consolidated ligand identification by mass spectrometry, defined S329 as the serine site enabling LFA-1-dependent lipid raft recruitment, and demonstrated in vivo tumor rejection requiring CD8+ T, NK cells, and DNAM-1+ dendritic cells.

    Evidence Mass spectrometry, reciprocal chimeric staining, S329 mutagenesis with lipid raft fractionation, in vivo ligand-transduced tumor rejection with depletion/KO

    PMID:15607800 PMID:15684041 PMID:15752754 PMID:16249389

    Open questions at the time
    • Ordering of serine/raft/tyrosine phosphorylation events not fully resolved
    • Cell-intrinsic vs APC contributions of CD226 not separated
  9. 2006 High

    Established mechanistic ordering by showing serine phosphorylation induces LFA-1 association which then carries CD226 into rafts, and extended CD226 function to mast cell degranulation synergy with FcεRI.

    Evidence LFA-1-deficient T cells with lipid raft fractionation, mast cell/eosinophil co-culture with pharmacological signaling inhibition

    PMID:16636013 PMID:16831868

    Open questions at the time
    • Kinase responsible for serine phosphorylation unidentified
    • Mast cell pathway relies on inhibitor specificity
  10. 2008 High

    Germline knockout established CD226 as an in vivo tumor immunosurveillance receptor and defined its context-specific requirement: costimulation for CD8+ T cells with nonprofessional APCs, and elimination of tumors lacking other NK-activating ligands.

    Evidence DNAM-1 KO mice in tumor transplant and carcinogen models, in vitro cytotoxicity and costimulation assays across APC types

    PMID:19029379 PMID:19029380

    Open questions at the time
    • Downstream transcriptional effectors not yet defined
    • Cytoplasmic signaling motif still uncharacterized at the residue level
  11. 2012 High

    Defined the competitive relationship with the inhibitory receptor TIGIT, showing TIGIT suppresses T cells partly by displacing CD226 from shared CD155.

    Evidence TIGIT shRNA knockdown, agonist/blocking mAb epistasis, cytokine and transcription factor measurement

    PMID:22427644

    Open questions at the time
    • Relative ligand affinities of CD226 vs TIGIT not quantified here
    • T cell-intrinsic TIGIT mechanism not fully separated
  12. 2015 High

    Delineated the cytoplasmic ITT-like motif signaling cascade (Grb2/Vav-1/PI3K/PLCγ1/Erk/Akt) driving cytotoxicity, and showed CD226 marks functionally distinct NK subsets and limits multiple myeloma.

    Evidence ITT-motif mutagenesis with Grb2 co-IP and downstream signaling assays, NK transcriptional profiling, Vk*MYC myeloma mouse model with depletion/blockade

    PMID:25818301 PMID:25825444 PMID:25893601 PMID:26552706

    Open questions at the time
    • Transcription factor terminus of the signaling cascade not yet identified
    • Link between adhesion-only and signaling functions partly unresolved
  13. 2018 High

    Provided the structural basis for ligand binding via tandem D1–D2 IgV domains, identified FOXO1 inactivation as a terminal signaling output, and established CD226 as an antagonist of TIGIT+ Treg suppressive function.

    Evidence Crystal structure with domain-deletion binding assays, CD226 KO with FOXO1 phosphorylation and pharmacological inhibition, Treg suppression assays in melanoma

    PMID:30046006 PMID:30504141 PMID:30591568

    Open questions at the time
    • Kinase linking CD226 to FOXO1 phosphorylation not pinpointed
    • Treg-disrupting mechanism partly correlative
  14. 2019 High

    Extended CD226 costimulatory function to small peritoneal macrophages as antigen-presenting cells required for CD4+ T cell priming.

    Evidence DNAM-1 KO mice, co-culture antigen presentation, adoptive SPM transfer, in vivo immunization

    PMID:30315271

    Open questions at the time
    • Molecular signaling of CD226 within macrophages not defined here
    • Ligand source during priming unspecified
  15. 2020 High

    Revealed multilayered regulation of CD226 abundance and competitive ligand binding: Y319-driven CBL-B ubiquitination/degradation, Eomes-mediated transcriptional repression, preferential competition for soluble CD155 over TIGIT/CD96, and TIGIT-blockade-induced Y322 phosphorylation, all shaping checkpoint blockade outcomes; also defined macrophage polarization roles.

    Evidence Y319 mutagenesis with CBL-B co-IP and proteasomal inhibition, Eomes manipulation with Cd226-/- mice and anti-PD-1, receptor-specific KO mice with sCD155 and affinity measurements, phospho-Y322 analysis, macrophage polarization in MI model

    PMID:32040157 PMID:32104514 PMID:32265229 PMID:33053330 PMID:33053331

    Open questions at the time
    • Integration of degradation and transcriptional control not unified
    • Macrophage CD226 ligand and signaling partly defined
  16. 2021 High

    Showed CD226 can regulate Treg function purely by sequestering CD155 from TIGIT—without CD226 intracellular signaling—thereby controlling the Akt-mTORC1/Foxp3 axis and Treg stability, and defined PPAR-γ downstream of CD226 in macrophages.

    Evidence DNAM-1-deficient Treg transfer in GvHD, Akt-mTORC1/Foxp3 assays, adipose macrophage KO with VAV1/AKT/FOXO1 phosphorylation and PPAR-γ inhibitor rescue

    PMID:34011606 PMID:34823548

    Open questions at the time
    • Generalizability of signaling-independent ligand competition across cell types unclear
    • PPAR-γ link relies on inhibitor rescue in single lab
  17. 2022 Medium

    Defined a stage-dependent requirement for CD226 in human Tfh differentiation, strong early and dispensable/inhibitory at the mature GC-Tfh stage.

    Evidence CD155-expressing artificial APC co-culture with anti-CD226 blockade, proliferation and Tfh marker assays

    PMID:35273617

    Open questions at the time
    • Blocking-antibody-based, single lab
    • Intracellular signaling driving stage-specific effects not mapped
  18. 2023 High

    Demonstrated via Treg-specific conditional deletion that the CD226/TIGIT balance on Tregs governs Treg stability and autoimmune diabetes incidence.

    Evidence Foxp3-Cre Treg-specific Cd226 KO in NOD mice, diabetes monitoring, TIGIT-Fc functional validation

    PMID:37625150

    Open questions at the time
    • Mechanistic coupling to systemic autoimmunity incomplete
    • Single disease model
  19. 2024 High

    Extended CD226 function to innate lymphoid cells, showing inducible CD226 enhances ILC2 effector function via PI3K/AKT and MAPK signaling and drives airway hyperreactivity.

    Evidence Anti-CD226 antibody, RNA-seq of sorted ILC2s, PI3K/AKT and MAPK assays, IL-33 and Alternaria AHR models in WT and Rag2-/- mice

    PMID:38244725

    Open questions at the time
    • ILC2 ligand source in airway not defined
    • Metabolic reprogramming mechanism incompletely mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the distinct CD226 phosphosites (Y319 degradation, Y322 signaling, S329 LFA-1/raft recruitment) are coordinately balanced to determine activation versus receptor turnover across cell types, and the kinase directly linking CD226 to FOXO1, remain unresolved.
  • No unified model integrating signaling vs degradation phosphosites
  • Direct CD226-to-FOXO1 kinase unidentified
  • Structural model of full signaling complex with LFA-1 lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098631 cell adhesion mediator activity 3 GO:0098772 molecular function regulator activity 3 GO:0060089 molecular transducer activity 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 1
Partners
CBLFYNGRB2ITGALNECTIN2PVRTIGIT

Evidence

Reading pass · 38 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 DNAM-1 (CD226) is a 65 kDa transmembrane glycoprotein with two immunoglobulin-like domains that is tyrosine-phosphorylated upon activation and functions as a signal-transducing adhesion molecule participating in primary adhesion during CTL-mediated cytotoxicity. Anti-DNAM-1 mAb inhibits T and NK cell-mediated cytotoxicity and blocks cytokine production by alloantigen-specific T cells. Monoclonal antibody blocking, immunoprecipitation, signal transduction analysis Immunity High 8673704
1985 TLiSA1 (CD226) is a T lineage-specific activation antigen whose antibody-mediated blockade from the beginning of mixed lymphocyte culture inhibits the induction of both CTL and anomalous killer (AK) cells from precursors, reducing CTL frequency and greatly reducing AK cell frequency under limiting dilution conditions, indicating a role in differentiation of cytotoxic effectors. Mixed lymphocyte culture with mAb blockade, limiting dilution analysis The Journal of experimental medicine Medium 2580933
1989 TGF-β suppresses TLiSA1 (CD226) surface expression and inhibits CTL and LAK cell differentiation in a dose-dependent manner; antibody to TGF-β reverses both effects, and anti-TLiSA1 antibody mimics TGF-β in inhibiting cytotoxic effector differentiation, linking TLiSA1 expression to the differentiation process. Mixed lymphocyte culture with TGF-β treatment, mAb blocking, anti-TGF-β rescue Immunology Medium 2541074
1997 TLiSA1/PTA1 (CD226) was cloned and identified as a novel immunoglobulin superfamily member with two V-set domains only. Identity between the T cell activation antigen TLiSA1 and platelet antigen PTA1 was established by immunological criteria, internal peptide sequencing, and RT-PCR of platelet transcript. Phorbol ester stimulates mRNA and surface expression, while combined phorbol ester and ionophore suppresses expression via a calcineurin-independent pathway. cDNA cloning, peptide sequencing, RT-PCR, flow cytometry, pharmacological perturbation The Journal of biological chemistry High 9268302
1999 LFA-1 physically associates with DNAM-1 in NK cells and anti-CD3-stimulated T cells, and serine phosphorylation of DNAM-1 plays a critical role in this association. Cross-linking of LFA-1 induces tyrosine phosphorylation of DNAM-1, for which the Fyn protein tyrosine kinase is responsible. DNAM-1-mediated cytotoxicity is defective in LFA-1-deficient (LAD syndrome) NK cells and is restored by genetic reconstitution of LFA-1 expression. Co-immunoprecipitation, genetic reconstitution, phosphorylation assays, cytotoxicity assays with LAD patient NK cells Immunity High 10591186
2003 CD226 mediates platelet adhesion to vascular endothelial cells; thrombin-activated (but not resting) platelets bind to intact HUVEC via CD226, and thrombin-induced platelet activation induces tyrosine phosphorylation of CD226. Mutant transfectant experiments demonstrated that tyrosine at residue 322 is critical for CD226 adhesive function. CD226 is also expressed on megakaryocytic cells and mediates their adhesion to HUVEC. mAb blocking adhesion assay, site-directed mutagenesis (Y322 mutant transfectants), phosphorylation assay The Journal of biological chemistry High 12847109
2003 Upon TCR antigen recognition, LFA-1 physically associates with CD226 (DNAM-1) and the protein tyrosine kinase Fyn. Lentiviral expression of mutant Y322F CD226 in naive CD4+ and CD8+ T cells inhibited LFA-1-mediated costimulatory signals for naive T cell proliferation and IL-12-independent Th1 differentiation. LFA-1, CD226, and Fyn are polarized at the immunological synapse upon CD3 stimulation. Lipid raft disruption inhibits LFA-1 costimulatory signaling in CD4+ but not CD8+ T cells. Lentiviral mutant transduction (Y322F), T cell proliferation assay, Th1 differentiation assay, immunological synapse imaging, lipid raft disruption The Journal of experimental medicine High 14676297
2004 Human CD155 (PVR) and CD112 (Nectin-2/PRR-2) were identified as ligands for human CD226. Ectopic expression of CD155 and/or CD112 on mouse BW5147 T cells increased their susceptibility to IL-2-activated T and NK cell-mediated cytotoxicity, which was specifically inhibited by anti-CD226 mAb. Ligation of CD226 and LFA-1 cooperates in triggering cytotoxicity and cytokine secretion. Ectopic expression/transfection, cytotoxicity assay, mAb blocking, binding affinity measurement International immunology High 15039383
2004 DNAM-1 (CD226) regulates monocyte transendothelial migration; PVR (CD155) is expressed at endothelial cell junctions and is the major DNAM-1 ligand on endothelial cells (Nectin-2 contributes less). Anti-DNAM-1 and anti-PVR mAbs blocked monocyte transmigration in vitro, arresting monocytes at the apical surface over intercellular junctions, indicating DNAM-1-PVR interaction occurs during the diapedesis step. Soluble DNAM-1-Fc binding assay, mAb blocking, transendothelial migration assay, confocal microscopy The Journal of experimental medicine High 15136589
2005 PVR and Nectin-2 were confirmed as DNAM-1 ligands by mass spectrometry identification of purified proteins and by demonstrating mutual staining between PVR-Fc/Nectin-2-Fc chimeric molecules and DNAM-1-expressing cells and vice versa. DNAM-1/PVR or Nectin-2 interaction enhanced NK-mediated lysis of tumor cells. Tryptic digestion and mass spectrometry, chimeric protein staining, cytotoxicity assay with mAb blocking Molecular immunology High 15607800
2005 DNAM-1 ligand-transduced RMA tumor cells were rejected in syngeneic mice in a CD8+ T cell- and NK cell-dependent manner generating CD8+ memory CTL. DNAM-1 is expressed on CD8α+ dendritic cells, and cross-linking DNAM-1 on these DCs induced their maturation and Th1 cell priming. Tumor rejection was abrogated in CD4+ T cell-depleted and MHC class II-deficient mice. Ligand transduction, in vivo tumor rejection assay, DC maturation assay, T cell depletion, KO mouse model Blood High 16249389
2005 Serine phosphorylation at residue 329 (S329) of DNAM-1 is required for LFA-1-dependent lipid raft recruitment of DNAM-1. Wild-type but not S329 mutant DNAM-1 associates with lipid rafts at peripheral supra-molecular activation clusters, and lipid raft association is necessary for tyrosine phosphorylation of DNAM-1, which is essential for LFA-1-mediated costimulatory signaling for naive T cell proliferation and differentiation. Site-directed mutagenesis (S329), lipid raft fractionation, immunological synapse imaging, T cell functional assays International immunology High 15684041
2005 Murine DNAM-1 and its PVR homologue were identified; they physically bind each other and ligand binding of murine DNAM-1 induces a costimulatory signal in antigen-specific CD8+ T cells. Binding assays, T cell costimulation assay Biochemical and biophysical research communications Medium 15752754
2006 Human mast cells and eosinophils express DNAM-1 (CD226) and its ligand Nectin-2 (CD112), respectively. CD226 engagement on mast cells synergizes with FcεRI and augments degranulation through a pathway involving Fyn, LAT, PLCγ2, and CD18. Blocking CD112 on eosinophils normalized the hyperactivity of IgE-activated mast cells co-cultured with eosinophils. This pathway is completely inhibited by linking IgE with IRp60 using a bispecific antibody. mAb blocking, co-culture assay, pharmacological inhibition of signaling intermediates, bispecific antibody The Journal of biological chemistry Medium 16831868
2006 Lipid raft recruitment of DNAM-1 in CD4+ T cells depends on LFA-1 expression; in LFA-1-deficient CD4+ T cells, TCR-mediated serine phosphorylation of DNAM-1 occurs but DNAM-1 does not associate with lipid rafts, indicating serine phosphorylation of DNAM-1 primarily induces physical association with LFA-1, which then carries DNAM-1 into lipid rafts. LFA-1-deficient mouse T cells, lipid raft fractionation, phosphorylation assay International immunology High 16636013
2008 DNAM-1-deficient mice show accelerated tumor development and mortality after transplantation of DNAM-1 ligand (CD155)-expressing Meth A fibrosarcoma cells. DNAM-1-deficient CTL and NK cells show significantly reduced cytotoxic activity against DNAM-1 ligand-expressing tumor cells in vitro. DNAM-1-deficient mice also develop significantly more fibrosarcoma and papilloma in response to chemical carcinogens MCA and DMBA, demonstrating an in vivo tumor immunosurveillance role. DNAM-1 knockout mice, tumor transplantation model, chemical carcinogen model, in vitro cytotoxicity assay The Journal of experimental medicine High 19029379
2008 CD8+ T cells require DNAM-1 for co-stimulation when antigen is presented by nonprofessional APCs but not dendritic cells. NK cells require DNAM-1 for elimination of tumor cells with paucity of other NK-activating ligands. DNAM-1-deficient mice generated from knockout model demonstrated these cell-type and context-specific requirements. DNAM-1 knockout mice, in vitro T cell co-stimulation assay, in vitro NK cytotoxicity assay, DC vs. non-professional APC comparison The Journal of experimental medicine High 19029380
2012 TIGIT exerts immunosuppressive effects on CD4+ T cells by competing with CD226 for binding to CD155. Knockdown of TIGIT by shRNA increased T-bet and IFN-γ expression; this increase was overcome by blocking CD226 signaling, demonstrating that TIGIT inhibits T cell function partly by displacing CD226 from its CD155 ligand. TIGIT also directly inhibits T cells in a T cell-intrinsic manner. shRNA knockdown of TIGIT, anti-TIGIT agonist mAb, anti-CD226 blocking mAb, cytokine/transcription factor measurement Journal of immunology High 22427644
2015 DNAM-1 controls NK cell-mediated cytotoxicity and cytokine production via a conserved tyrosine- and asparagine-based ITT-like motif in its cytoplasmic domain. Upon Src kinase-mediated phosphorylation of this motif, DNAM-1 binds adaptor Grb2, leading to activation of Vav-1, PI3K, and PLCγ1, as well as Erk and Akt kinases and calcium flux. DNAM-1 signaling also enhances cytotoxicity by increasing actin polymerization and granule polarization. DNAM-1-mediated adhesion is signal-independent and insufficient alone for cytotoxicity. Site-directed mutagenesis of ITT-like motif, co-immunoprecipitation of Grb2, downstream signaling assays (Erk, Akt, calcium flux), actin polymerization assay, granule polarization assay The Journal of experimental medicine High 26552706
2015 DNAM-1 expression identifies two functionally distinct NK cell subsets: DNAM-1+ NK cells produce high levels of inflammatory cytokines, have enhanced IL-15 signaling, and proliferate vigorously; DNAM-1- NK cells differentiate from DNAM-1+ cells, express more NK receptor-related genes, and produce higher levels of MIP1 chemokines. Transcriptional profiling, functional cytokine production assay, proliferation assay, IL-15 signaling assay Cell reports Medium 25818301
2015 In educated NK cells, upon target cell recognition, the conformational state of LFA-1 changes and both active LFA-1 and DNAM-1 rapidly colocalize at the immune synapse. DNAM-1 expression correlates with the quantity and quality of inhibitory input by HLA class I-specific KIRs and CD94/NKG2A, and with the magnitude of functional responses. Flow cytometry, live imaging, functional cytotoxicity correlation analysis Journal of immunology Medium 25825444
2015 CD226 is required for immunosurveillance and therapy of multiple myeloma; CD226 limits spontaneous MM development in Vk*MYC transgenic mice. The anti-myeloma immune response is mediated by both NK and CD8+ T cells through perforin and IFN-γ pathways. CD226 expression is also required for optimal antimyeloma efficacy of cyclophosphamide and bortezomib. Cd226 mutant mice crossed with Vk*MYC MM model, NK/T cell depletion, perforin/IFN-γ blockade, drug treatment The Journal of clinical investigation High 25893601
2018 CD226 binding to CD155 is mediated by a unique side-by-side arrangement of two tandem IgV domains (D1 and D2). Crystal structure of mCD226-ecto revealed that D1 forms the conserved binding interface with CD155-D1, while D2 provides structural support and forms direct interactions with CD155. Deletion of D2 substantially reduced CD226 binding efficacy to CD155. Crystal structure determination (X-ray crystallography), deletion mutant binding assay Proceedings of the National Academy of Sciences of the United States of America High 30591568
2018 CD226 regulates NK cell antitumor responses via phosphorylation-mediated inactivation of transcription factor FOXO1. Engagement of CD155 ligand results in phosphorylation of FOXO1 downstream of CD226. CD226 deficiency or anti-CD226 antibody blockade impaired cytotoxicity with concomitant compromised inactivation of FOXO1. Inhibitors of FOXO1 phosphorylation abrogated CD226-mediated signaling and effector responses. CD226-deficient mice, gene expression analysis, in vitro cytotoxicity/stimulation assay, FOXO1 phosphorylation assay, pharmacological inhibitors Proceedings of the National Academy of Sciences of the United States of America High 30504141
2018 CD226 opposes TIGIT to disrupt Treg suppressive function in melanoma; TIGIT+ Tregs are highly suppressive and stable while CD226 disrupts Treg suppression and stability. A high TIGIT/CD226 ratio in Tregs correlates with increased Treg frequencies in tumors. Flow cytometry of Tregs from melanoma patients and tumors, functional suppression assay, mAb blocking of TIGIT and CD226 JCI insight Medium 30046006
2019 DNAM-1 on small peritoneal macrophages (SPMs) is required for CD4+ T cell co-stimulation; SPMs but not large peritoneal macrophages (LPMs) express DNAM-1 and have antigen-presenting capacity. DNAM-1 deficiency on SPMs or blockade of DNAM-1/ligand interaction impaired CD4+ T cell priming. Wild-type but not DNAM-1-deficient SPMs enhanced T and B cell responses in vivo upon adoptive transfer. DNAM-1 KO mice, co-culture antigen presentation assay, adoptive SPM transfer, in vivo immunization Scientific reports High 30315271
2020 Tumor-derived CD155 initiates phosphorylation of CD226 at tyrosine 319 (Y319) by Src kinases, which enables ubiquitination of CD226 by the E3 ligase CBL-B, followed by internalization and proteasomal degradation of CD226. Mutation of Y319 led to increased CD226 surface expression, enhanced anti-tumor immunity, and improved immune checkpoint blockade efficacy. Y319 mutagenesis, phosphorylation assay, CBL-B co-immunoprecipitation, proteasomal inhibition, in vivo tumor models Immunity High 33053330
2020 Loss of CD226 expression on CD8+ T cells is driven by the transcriptional regulator Eomesodermin (Eomes) through an antigen-specific mechanism. CD226-negative CD8+ T cells exhibit reduced LFA-1 activation, altered TCR signaling, and a distinct transcriptomic program. CD226-deficient CD8+ TILs fail to respond to anti-PD-1, and immune checkpoint blockade efficacy was hampered in Cd226-/- mice. Transcriptome analysis, Eomes overexpression/knockdown, Cd226-/- mice, anti-PD-1 treatment, LFA-1 activation assay Immunity High 33053331
2020 Soluble CD155 (sCD155) secreted by tumor cells inhibits DNAM-1-mediated NK cell degranulation and promotes lung colonization of B16/BL6 melanoma; in vivo the effect required DNAM-1 (not TIGIT or CD96). DNAM-1 has greater affinity than TIGIT and CD96 for sCD155, indicating preferential competitive binding. sCD155-expressing tumor injection in KO mice (DNAM-1, TIGIT, CD96), in vitro degranulation assay, binding affinity measurement The Journal of experimental medicine High 32040157
2020 Anti-TIGIT treatment selectively promotes CD226 phosphorylation at tyrosine 322 in CD226hiCD8+ T cells, and CD226 agonist antibody augments the effect of TIGIT blockade on CD8+ T cell responses. CD226loCD8+ T cells accumulate at the tumor site with exhausted phenotype. Flow cytometry, phospho-Y322 analysis after anti-TIGIT treatment, CD226 agonist antibody functional assay Cancer immunology research Medium 32265229
2020 CD226 deletion in mice improves post-myocardial infarction healing by favoring macrophage M2 polarization and suppressing M1 polarization. In vitro, CD226 deletion in bone marrow-derived macrophages potentiated M2 and suppressed M1 polarization. CD226 deletion also restrained inflammatory monocyte mobilization from spleen to blood. CD226 KO mice with coronary ligation model, bone marrow-derived macrophage polarization assay, flow cytometry of monocyte subsets Theranostics Medium 32104514
2021 DNAM-1 competes with TIGIT in binding to their common ligand CD155, thereby regulating TIGIT signaling to down-regulate Treg cell function without requiring DNAM-1-mediated intracellular signaling. DNAM-1 deficiency augments TIGIT signaling, which inhibits Akt-mTORC1 pathway activation, maintaining Foxp3 expression and Treg function under inflammatory conditions. Transfer of DNAM-1-deficient Treg cells ameliorated graft-versus-host disease better than wild-type Tregs. DNAM-1-deficient Treg transfer, GvHD model, Akt-mTORC1 signaling assay, Foxp3 stability assay, TIGIT signaling measurement Proceedings of the National Academy of Sciences of the United States of America High 34011606
2021 CD226 deficiency on adipose tissue macrophages (ATMs) decreases phosphorylation of VAV1, AKT, and FOXO1 and upregulates PPAR-γ, thereby inhibiting macrophage M1 polarization. Administration of a PPAR-γ inhibitor restored M1 phenotype in CD226KO ATMs, placing PPAR-γ downstream of CD226 signaling in macrophage polarization. CD226 KO mice, HFD obesity model, phosphorylation assays (VAV1, AKT, FOXO1), PPAR-γ inhibitor rescue experiment Journal of translational medicine Medium 34823548
2022 CD226 signals promote the early phase of human Tfh cell differentiation; blocking CD226 potently inhibited proliferation and Tfh marker expression of naive CD4+ T cells and Tfh precursors stimulated with CD155-expressing APCs. In contrast, mature GC-Tfh cells require only weak CD226 signals, and attenuating CD226 rather increased CXCR5, ICOS, and IL-21 expression, indicating the requirement for CD226 wanes as Tfh cells mature. CD155-expressing artificial APC co-culture, anti-CD226 blocking antibody, proliferation assay, Tfh marker expression assay Frontiers in immunology Medium 35273617
2023 Treg-specific Cd226 deletion (TregΔCd226 mice) decreased insulitis and diabetes incidence in NOD mice. CD226-deficient pancreatic Tregs had increased TIGIT expression. NOD splenocytes treated with TIGIT-Fc fusion protein showed reduced T cell proliferation and IFN-γ production, indicating CD226/TIGIT imbalance on Tregs contributes to Treg instability. Conditional Treg-specific KO (Foxp3-Cre), diabetes incidence monitoring, TIGIT-Fc fusion protein treatment, proliferation and cytokine assays Diabetes High 37625150
2024 CD226 is inducibly expressed in activated ILC2s and enhances their cytokine secretion and effector functions. Mechanistically, CD226 alters intracellular metabolism and enhances PI3K/AKT and MAPK signaling pathways in ILC2s. Blocking CD226 ameliorates ILC2-dependent airway hyperreactivity in IL-33 and Alternaria alternata-induced models. Anti-CD226 antibody treatment, RNA sequencing of sorted ILC2s, PI3K/AKT and MAPK signaling assay, in vivo AHR mouse models (WT and Rag2-/- mice) The Journal of allergy and clinical immunology High 38244725
2014 The alphaherpesvirus gD glycoprotein causes degradation and down-regulation of CD112 (a DNAM-1 ligand), reducing DNAM-1 binding to infected cells and suppressing DNAM-1-mediated NK cell degranulation and lysis of PRV- or HSV-2-infected cells. Viral infection/transfection with gD expression, flow cytometry of CD112, NK degranulation assay, cytotoxicity assay Proceedings of the National Academy of Sciences of the United States of America Medium 25352670
2016 Mouse CMV m20.1 protein retains PVR (DNAM-1 ligand) in the endoplasmic reticulum and promotes its degradation. A MCMV mutant lacking m20.1 was attenuated in normal but not DNAM-1 KO mice. This attenuation was partially reversed by NK cell depletion and abolished by simultaneous depletion of mononuclear phagocytes, indicating that inflammatory monocytes together with NK cells control CMV through the DNAM-1-PVR pathway. MCMV m20.1 deletion mutant, DNAM-1 KO mice, cell depletion, iNOS inhibition, CCL2 blocking The Journal of experimental medicine High 27503073

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 DNAM-1, a novel adhesion molecule involved in the cytolytic function of T lymphocytes. Immunity 524 8673704
2012 The TIGIT/CD226 axis regulates human T cell function. Journal of immunology (Baltimore, Md. : 1950) 391 22427644
2008 DNAM-1 promotes activation of cytotoxic lymphocytes by nonprofessional antigen-presenting cells and tumors. The Journal of experimental medicine 283 19029380
2007 The requirement for DNAM-1, NKG2D, and NKp46 in the natural killer cell-mediated killing of myeloma cells. Cancer research 275 17875681
2004 Functional characterization of DNAM-1 (CD226) interaction with its ligands PVR (CD155) and nectin-2 (PRR-2/CD112). International immunology 226 15039383
2008 Accelerated tumor growth in mice deficient in DNAM-1 receptor. The Journal of experimental medicine 222 19029379
2004 DNAM-1 and PVR regulate monocyte migration through endothelial junctions. The Journal of experimental medicine 219 15136589
2005 Expression of the DNAM-1 ligands, Nectin-2 (CD112) and poliovirus receptor (CD155), on dendritic cells: relevance for natural killer-dendritic cell interaction. Blood 215 16304049
2003 CD226 (DNAM-1) is involved in lymphocyte function-associated antigen 1 costimulatory signal for naive T cell differentiation and proliferation. The Journal of experimental medicine 208 14676297
1999 Physical and functional association of LFA-1 with DNAM-1 adhesion molecule. Immunity 198 10591186
2011 Decreased expression of DNAM-1 on NK cells from acute myeloid leukemia patients. Immunology and cell biology 184 21383766
2022 TIGIT-CD226-PVR axis: advancing immune checkpoint blockade for cancer immunotherapy. Journal for immunotherapy of cancer 180 35379739
2019 DNAM-1 and the TIGIT/PVRIG/TACTILE Axis: Novel Immune Checkpoints for Natural Killer Cell-Based Cancer Immunotherapy. Cancers 175 31234588
2018 CD226 opposes TIGIT to disrupt Tregs in melanoma. JCI insight 162 30046006
2009 DNAM-1/CD155 interactions promote cytokine and NK cell-mediated suppression of poorly immunogenic melanoma metastases. Journal of immunology (Baltimore, Md. : 1950) 159 20008292
2020 Characterization of Human NK Cell-Derived Exosomes: Role of DNAM1 Receptor In Exosome-Mediated Cytotoxicity Against Tumor. Cancers 142 32178479
2020 CD155 on Tumor Cells Drives Resistance to Immunotherapy by Inducing the Degradation of the Activating Receptor CD226 in CD8+ T Cells. Immunity 133 33053330
2020 Eomes-Dependent Loss of the Co-activating Receptor CD226 Restrains CD8+ T Cell Anti-tumor Functions and Limits the Efficacy of Cancer Immunotherapy. Immunity 122 33053331
2011 DNAM-1 ligand expression on Ag-stimulated T lymphocytes is mediated by ROS-dependent activation of DNA-damage response: relevance for NK-T cell interaction. Blood 120 21406724
2014 The DNA Damage Response: A Common Pathway in the Regulation of NKG2D and DNAM-1 Ligand Expression in Normal, Infected, and Cancer Cells. Frontiers in immunology 119 24432022
2015 DNAM-1 controls NK cell activation via an ITT-like motif. The Journal of experimental medicine 118 26552706
2013 DNAM-1 control of natural killer cells functions through nectin and nectin-like proteins. Immunology and cell biology 117 24343663
2005 PVR (CD155) and Nectin-2 (CD112) as ligands of the human DNAM-1 (CD226) activating receptor: involvement in tumor cell lysis. Molecular immunology 116 15607800
2005 Tumor rejection by the poliovirus receptor family ligands of the DNAM-1 (CD226) receptor. Blood 111 16249389
2009 DNAX accessory molecule-1 (CD226) promotes human hepatocellular carcinoma cell lysis by Vgamma9Vdelta2 T cells. European journal of immunology 110 19404979
2015 Immunosurveillance and therapy of multiple myeloma are CD226 dependent. The Journal of clinical investigation 109 25893601
1985 TLiSA1, a human T lineage-specific activation antigen involved in the differentiation of cytotoxic T lymphocytes and anomalous killer cells from their precursors. The Journal of experimental medicine 109 2580933
2015 DNAM-1 expression marks an alternative program of NK cell maturation. Cell reports 108 25818301
2008 NK cells recognize and lyse Ewing sarcoma cells through NKG2D and DNAM-1 receptor dependent pathways. Molecular immunology 107 18657862
2021 TIGIT/CD226 Axis Regulates Anti-Tumor Immunity. Pharmaceuticals (Basel, Switzerland) 103 33670993
2010 NKp46 and DNAM-1 NK-cell receptors drive the response to human cytomegalovirus-infected myeloid dendritic cells overcoming viral immune evasion strategies. Blood 97 21030563
2003 CD226 mediates platelet and megakaryocytic cell adhesion to vascular endothelial cells. The Journal of biological chemistry 89 12847109
2015 Differential expression of ligands for NKG2D and DNAM-1 receptors by epithelial ovarian cancer-derived exosomes and its influence on NK cell cytotoxicity. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 83 26563374
2015 Coordinated expression of DNAM-1 and LFA-1 in educated NK cells. Journal of immunology (Baltimore, Md. : 1950) 80 25825444
2020 Tumor-derived soluble CD155 inhibits DNAM-1-mediated antitumor activity of natural killer cells. The Journal of experimental medicine 79 32040157
2020 CD226: An Emerging Role in Immunologic Diseases. Frontiers in cell and developmental biology 72 32850777
2020 CD226hiCD8+ T Cells Are a Prerequisite for Anti-TIGIT Immunotherapy. Cancer immunology research 70 32265229
2020 DNAM1 and 2B4 Costimulatory Domains Enhance the Cytotoxicity of Anti-GPC3 Chimeric Antigen Receptor-Modified Natural Killer Cells Against Hepatocellular Cancer Cells in vitro. Cancer management and research 69 32440221
2011 Activating NK cell receptor expression/function (NKp30, NKp46, DNAM-1) during chronic viraemic HCV infection is associated with the outcome of combined treatment. European journal of immunology 69 21695691
2020 TIGIT blockade enhances functionality of peritoneal NK cells with altered expression of DNAM-1/TIGIT/CD96 checkpoint molecules in ovarian cancer. Oncoimmunology 62 33224630
2006 Mast cell costimulation by CD226/CD112 (DNAM-1/Nectin-2): a novel interface in the allergic process. The Journal of biological chemistry 61 16831868
2015 NKG2D and DNAM-1 Ligands: Molecular Targets for NK Cell-Mediated Immunotherapeutic Intervention in Multiple Myeloma. BioMed research international 59 26161387
2010 Non-synonymous variant (Gly307Ser) in CD226 is associated with susceptibility to multiple autoimmune diseases. Rheumatology (Oxford, England) 59 20338887
2016 Altered expression of CD226 and CD96 on natural killer cells in patients with pancreatic cancer. Oncotarget 57 27626490
2018 CD226 regulates natural killer cell antitumor responses via phosphorylation-mediated inactivation of transcription factor FOXO1. Proceedings of the National Academy of Sciences of the United States of America 55 30504141
2015 Nitric oxide donors increase PVR/CD155 DNAM-1 ligand expression in multiple myeloma cells: role of DNA damage response activation. BMC cancer 52 25609078
2005 Identification and characterization of murine DNAM-1 (CD226) and its poliovirus receptor family ligands. Biochemical and biophysical research communications 51 15752754
2019 DNAM-1 Activating Receptor and Its Ligands: How Do Viruses Affect the NK Cell-Mediated Immune Surveillance during the Various Phases of Infection? International journal of molecular sciences 50 31366013
1989 TGF beta down-regulates TLiSA1 expression and inhibits the differentiation of precursor lymphocytes into CTL and LAK cells. Immunology 50 2541074
2021 DNAM-1 versus TIGIT: competitive roles in tumor immunity and inflammatory responses. International immunology 49 34694361
2017 Expression of CD226 is associated to but not required for NK cell education. Nature communications 49 28561023
2020 Boosting Natural Killer Cell-Mediated Targeting of Sarcoma Through DNAM-1 and NKG2D. Frontiers in immunology 48 32082316
2014 UPR decreases CD226 ligand CD155 expression and sensitivity to NK cell-mediated cytotoxicity in hepatoma cells. European journal of immunology 48 25209846
2012 CD226 Gly307Ser association with multiple autoimmune diseases: a meta-analysis. Human immunology 48 23073294
2016 Loss of DNAM-1 ligand expression by acute myeloid leukemia cells renders them resistant to NK cell killing. Oncoimmunology 47 27622064
2023 TIGIT can inhibit T cell activation via ligation-induced nanoclusters, independent of CD226 co-stimulation. Nature communications 46 37596248
2014 Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells. Proceedings of the National Academy of Sciences of the United States of America 46 25352670
2010 Loss of DNAM-1 contributes to CD8+ T-cell exhaustion in chronic HIV-1 infection. European journal of immunology 46 20201043
2005 Requirement of the serine at residue 329 for lipid raft recruitment of DNAM-1 (CD226). International immunology 46 15684041
2021 Hitting the complexity of the TIGIT-CD96-CD112R-CD226 axis for next-generation cancer immunotherapy. BMB reports 44 33298247
2018 Binding mode of the side-by-side two-IgV molecule CD226/DNAM-1 to its ligand CD155/Necl-5. Proceedings of the National Academy of Sciences of the United States of America 42 30591568
2016 Inflammatory monocytes and NK cells play a crucial role in DNAM-1-dependent control of cytomegalovirus infection. The Journal of experimental medicine 42 27503073
2015 Drug-induced hyperploidy stimulates an antitumor NK cell response mediated by NKG2D and DNAM-1 receptors. Oncoimmunology 42 27057443
2020 CD226 deletion improves post-infarction healing via modulating macrophage polarization in mice. Theranostics 39 32104514
2020 Nutlin-3a Enhances Natural Killer Cell-Mediated Killing of Neuroblastoma by Restoring p53-Dependent Expression of Ligands for NKG2D and DNAM-1 Receptors. Cancer immunology research 38 33303573
2014 DNAM-1-based chimeric antigen receptors enhance T cell effector function and exhibit in vivo efficacy against melanoma. Cancer immunology, immunotherapy : CII 38 25549845
2021 DNAM-1 regulates Foxp3 expression in regulatory T cells by interfering with TIGIT under inflammatory conditions. Proceedings of the National Academy of Sciences of the United States of America 37 34011606
2018 Interaction of PVR/PVRL2 with TIGIT/DNAM-1 as a novel immune checkpoint axis and therapeutic target in cancer. Mammalian genome : official journal of the International Mammalian Genome Society 36 30132062
2012 Cancer immunotherapy using NKG2D and DNAM-1 systems. Anticancer research 36 22641658
2020 Higher TIGIT+CD226- γδ T cells in Patients with Acute Myeloid Leukemia. Immunological investigations 35 32819181
2021 BCL9 regulates CD226 and CD96 checkpoints in CD8+ T cells to improve PD-1 response in cancer. Signal transduction and targeted therapy 33 34417435
2022 Emergence of the CD226 Axis in Cancer Immunotherapy. Frontiers in immunology 32 35812451
2015 Expression of DNAM-1 (CD226) on inflammatory monocytes. Molecular immunology 32 26675069
2012 Critical role of the adhesion receptor DNAX accessory molecule-1 (DNAM-1) in the development of inflammation-driven dermal fibrosis in a mouse model of systemic sclerosis. Annals of the rheumatic diseases 32 23161903
2020 Characterization of the DNAM-1, TIGIT and TACTILE Axis on Circulating NK, NKT-Like and T Cell Subsets in Patients with Acute Myeloid Leukemia. Cancers 31 32764229
1997 TLiSA1 (PTA1) activation antigen implicated in T cell differentiation and platelet activation is a member of the immunoglobulin superfamily exhibiting distinctive regulation of expression. The Journal of biological chemistry 31 9268302
2022 DNAM-1-chimeric receptor-engineered NK cells, combined with Nutlin-3a, more effectively fight neuroblastoma cells in vitro: a proof-of-concept study. Frontiers in immunology 29 35967339
2020 Characteristic of TIGIT and DNAM-1 Expression on Foxp3+ γδ T Cells in AML Patients. BioMed research international 29 32802845
2019 CD226 attenuates Treg suppressive capacity via CTLA-4 and TIGIT during EAE. Immunologic research 29 31919790
2006 LFA-1-dependent lipid raft recruitment of DNAM-1 (CD226) in CD4+ T cell. International immunology 29 16636013
2014 CD226 (DNAM-1) is associated with susceptibility to juvenile idiopathic arthritis. Annals of the rheumatic diseases 28 25057181
2003 The expression, regulation and adhesion function of a novel CD molecule, CD226, on human endothelial cells. Life sciences 27 12941439
2022 CD226 and TIGIT Cooperate in the Differentiation and Maturation of Human Tfh Cells. Frontiers in immunology 26 35273617
2019 Human peripheral blood DNAM-1neg NK cells are a terminally differentiated subset with limited effector functions. Blood advances 26 31167820
2015 'Emergency exit' of bone-marrow-resident CD34(+)DNAM-1(bright)CXCR4(+)-committed lymphoid precursors during chronic infection and inflammation. Nature communications 26 26436997
2024 Blocking CD226 regulates type 2 innate lymphoid cell effector function and alleviates airway hyperreactivity. The Journal of allergy and clinical immunology 25 38244725
2024 Revisiting T-cell adhesion molecules as potential targets for cancer immunotherapy: CD226 and CD2. Experimental & molecular medicine 24 39349829
2023 DNAM-1 chimeric receptor-engineered NK cells: a new frontier for CAR-NK cell-based immunotherapy. Frontiers in immunology 23 37359555
2023 Treg-Specific CD226 Deletion Reduces Diabetes Incidence in NOD Mice by Improving Regulatory T-Cell Stability. Diabetes 23 37625150
2020 CD226 Attenuates Treg Proliferation via Akt and Erk Signaling in an EAE Model. Frontiers in immunology 23 32983109
2022 Human allogenic γδ T cells kill patient-derived glioblastoma cells expressing high levels of DNAM-1 ligands. Oncoimmunology 22 36338147
2018 Selective DNAM-1 expression on small peritoneal macrophages contributes to CD4+ T cell costimulation. Scientific reports 22 30315271
2024 TGF-β-mediated crosstalk between TIGIT+ Tregs and CD226+CD8+ T cells in the progression and remission of type 1 diabetes. Nature communications 21 39406740
2019 Diminished cytolytic activity of γδ T cells with reduced DNAM-1 expression in neuroblastoma patients. Clinical immunology (Orlando, Fla.) 21 30999035
2019 CD226 deficiency on regulatory T cells aggravates renal fibrosis via up-regulation of Th2 cytokines through miR-340. Journal of leukocyte biology 21 31802539
2021 CD226 knockout alleviates high-fat diet induced obesity by suppressing proinflammatory macrophage phenotype. Journal of translational medicine 20 34823548
2018 Human NK Cells Lyse Th2-Polarizing Dendritic Cells via NKp30 and DNAM-1. Journal of immunology (Baltimore, Md. : 1950) 20 30120122
2021 Expansion of circulating peripheral TIGIT+CD226+ CD4 T cells with enhanced effector functions in dermatomyositis. Arthritis research & therapy 19 33413573
2014 XLP1 inhibitory effect by 2B4 does not affect DNAM-1 and NKG2D activating pathways in NK cells. European journal of immunology 19 24496997
2012 Association between the CD226 rs763361 polymorphism and susceptibility to autoimmune diseases: a meta-analysis. Lupus 19 22941566

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