Affinage

LILRB1

Leukocyte immunoglobulin-like receptor subfamily B member 1 · UniProt Q8NHL6

Length
650 aa
Mass
70.8 kDa
Annotated
2026-04-28
100 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

LILRB1 (ILT2/CD85j/LIR1) is a broadly expressed inhibitory immunoreceptor that recognizes classical and non-classical MHC class I molecules—including HLA-A/B/C, HLA-E, HLA-F, HLA-G, and the HCMV homolog UL18—through its D1D2 extracellular immunoglobulin domains, with highest affinity for HLA-G and particularly its dimeric form, and transmits inhibitory signals by recruiting SHP-1 phosphatase via cytoplasmic ITIM motifs (PMID:12853576, PMID:11169396, PMID:31273318). On NK cells, LILRB1 engagement blocks lytic granule polarization, MTOC reorientation, F-actin accumulation at the immunological synapse, calcium mobilization, and IFN-γ production; on CD8+ T cells it inhibits TCR-driven activation on a population distinct from PD-1+ cells; and on macrophages it functions as a phagocytosis checkpoint whose disruption potentiates tumor cell engulfment in vitro and in vivo (PMID:19841038, PMID:18684926, PMID:31253728, PMID:29180808, PMID:36389667). Plasmodium falciparum RIFIN proteins structurally mimic MHC class I to engage both the D1D2 and D3D4 domains of LILRB1, suppressing NK cell perforin mobilization and representing a pathogen immune-evasion strategy; naturally occurring LILRB1 D3D4 domain insertions into immunoglobulin genes generate RIFIN-specific antibodies in malaria-exposed individuals (PMID:32650338, PMID:33790470). Beyond canonical immune inhibition, LILRB1 forms a complex with LDLR and LDLRAP1 to facilitate LDL/cholesterol uptake in multiple myeloma cells, linking it to ferroptosis resistance through maintenance of intracellular squalene levels (PMID:38982045).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1999 Medium

    Establishing the molecular identity of the CD85j antigen as LILRB1/ILT2, an inhibitory Ig-superfamily receptor on multiple immune lineages, provided the foundation for all subsequent mechanistic work on this receptor.

    Evidence Affinity purification, tryptic peptide sequencing, and transfectant staining with anti-CD85 mAbs

    PMID:10380908

    Open questions at the time
    • Single-method identification without functional signaling readout
    • Expression pattern described by flow cytometry alone
  2. 2000 High

    Demonstrating that LILRB1 binds the non-classical molecule HLA-F expanded the receptor's ligand repertoire beyond classical MHC class I, raising the question of how broadly LILRB1 surveys MHC diversity.

    Evidence HLA-F tetramer staining, ILT2 transfection into non-binding cells, SPR confirmation

    PMID:11169396

    Open questions at the time
    • Functional consequence of HLA-F engagement on immune cell signaling not tested
    • Affinity comparison with classical MHC I not performed
  3. 2003 High

    Quantitative SPR measurements established that LILRB1 binds a broad panel of classical and non-classical MHC class I molecules with systematically higher affinity than LILRB2, and preferentially recognizes HLA-G, while competing with CD8 for MHC binding—defining LILRB1's dual inhibitory mechanism (ITIM signaling plus CD8 displacement).

    Evidence Surface plasmon resonance Kd measurements across multiple MHC I ligands; competition assays with CD8

    PMID:12853576

    Open questions at the time
    • CD8 competition demonstrated in vitro but not validated in T cell coculture
    • Contribution of CD8 displacement versus ITIM signaling to inhibition not quantified
  4. 2002 High

    Showing that LILRB1 ligation recruits SHP-1 and inhibits TCR/CD3-driven proliferation in Sézary cells provided the first direct evidence of the receptor's inhibitory signaling mechanism in T cells.

    Evidence SHP-1 recruitment assay, CD3/TCR stimulation proliferation assay, apoptosis comparison in CTCL cell lines

    PMID:12130517

    Open questions at the time
    • Downstream substrates of SHP-1 in LILRB1 signaling not identified
    • Studied in malignant CTCL lines; relevance to normal T cells assumed but not shown
  5. 2005 Medium

    The finding that HLA-G upregulates LILRB1 surface expression on APCs, NK cells, and T cells revealed a positive feedback loop between ligand and receptor that could amplify immune suppression.

    Evidence Flow cytometry of ILT2 expression after HLA-G exposure across multiple cell types

    PMID:15670976

    Open questions at the time
    • Single method (flow cytometry); transcriptional versus post-translational mechanism of upregulation not resolved
    • Functional consequence of upregulation on inhibitory signaling threshold not tested
  6. 2007 High

    Continuous LILRB1 ligation during DC differentiation was shown to modulate DC function—suppressing cytokine secretion, conferring apoptosis resistance, and promoting regulatory T cell induction—extending the receptor's role from acute inhibition to shaping APC programming.

    Evidence LILRB1 ligation during monocyte-to-DC differentiation, cytokine ELISA, apoptosis assay, MLR, antibody blockade

    PMID:18094328

    Open questions at the time
    • Signaling intermediates linking LILRB1 to DC programming not identified
    • In vivo relevance of sustained LILRB1 ligation during DC differentiation not tested
  7. 2008 High

    Demonstrating that LILRB1–HLA class I engagement inhibits IFN-γ at the transcriptional and protein level in NK cells, and that blocking this interaction increases IFN-γ in NK/DC cocultures, defined LILRB1 as a direct suppressor of NK cell effector cytokine output.

    Evidence NK stimulation assays with HLA I-expressing targets, IFN-γ mRNA/protein/secretion quantification, ILT2 blocking antibody

    PMID:18684926

    Open questions at the time
    • Signaling intermediates between SHP-1 and IFN-γ transcription not mapped
    • Relative contribution of LILRB1 versus KIR-mediated inhibition of IFN-γ not addressed
  8. 2009 High

    Detailed imaging of the NK cell immunological synapse revealed that LILRB1–HLA-G engagement specifically blocks granule polarization, MTOC reorientation, F-actin accumulation, and calcium flux without affecting activating receptor recruitment, mechanistically dissecting which synapse events LILRB1 controls.

    Evidence NK cell/target synapse imaging, granule polarization, MTOC localization, F-actin staining, calcium mobilization assays

    PMID:19841038

    Open questions at the time
    • Molecular link between SHP-1 activity and cytoskeletal rearrangement at the synapse not defined
    • Whether LILRB1 inhibits synapse formation cooperatively with other inhibitory receptors not tested
  9. 2016 Medium

    Showing that HLA class Ia dimers and interferon-induced noncanonical HLA conformers disproportionately enhance LILRB1 binding established ligand quaternary structure as a physiological regulator of LILRB1 avidity.

    Evidence LILRB1-Fc fusion binding, LILRB1-ζ chimera reporter, HLA-I transfectants, IFN-treated monocytes

    PMID:27109306

    Open questions at the time
    • Single lab study; independent replication needed
    • Structural basis for preferential dimer recognition not resolved at atomic level
  10. 2017 High

    Identification of MHC class I–LILRB1 as a macrophage phagocytosis checkpoint parallel to CD47–SIRPα fundamentally expanded LILRB1's role from lymphocyte inhibition to myeloid innate immunity and tumor immune evasion.

    Evidence In vitro and in vivo phagocytosis assays, LILRB1 knockdown/blockade, β2M manipulation on cancer cells, TAM expression analysis

    PMID:29180808

    Open questions at the time
    • Relative contribution of LILRB1 versus SIRPα to total 'don't eat me' signal not quantified in vivo
    • Whether LILRB1 engages additional non-MHC I ligands on tumor cells not excluded
  11. 2018 High

    Demonstrating that LILRB1 polymorphisms and N-linked glycosylation differentially alter binding to UL18 versus classical MHC I (but not HLA-G) linked host genetic variation to HCMV immune evasion efficiency.

    Evidence LILRB1 variant expression in NK models, binding assays with UL18/MHC I/HLA-G, glycosylation site mutagenesis, transplant cohort association

    PMID:29528338

    Open questions at the time
    • Population-level impact of LILRB1 polymorphisms on CMV control needs larger cohort validation
    • Structural basis for glycan-mediated differential ligand recognition not determined
  12. 2019 High

    Structural determination of LILRB1's four-domain architecture in complex with HLA-G1 revealed that D1D2 mediates ligand binding while D3D4 serves as a scaffold, and that dimeric HLA-G1 engages LILRB1 in a manner that potentiates inhibitory signaling, resolving a long-standing question about domain utilization.

    Evidence X-ray crystallography of four-domain LILRB1 and LILRB1–HLA-G1 complex

    PMID:31273318

    Open questions at the time
    • Full-length receptor structure including transmembrane and cytoplasmic ITIM domains not resolved
    • Dynamics of receptor clustering upon dimer engagement not captured
  13. 2019 Medium

    Characterization of LILRB1 as a checkpoint on late-differentiated CD8+ effector T cells distinct from PD-1, with functional inhibition by HLA-G reversible by blocking antibodies, positioned LILRB1 as a non-redundant immunotherapy target.

    Evidence Flow cytometry of CD8+ T cell subsets, BiTE stimulation assays, HLA-G engagement, dual LILRB1/PD-1 blockade experiments; ex vivo TIL functional assays

    PMID:31253728 PMID:31451484

    Open questions at the time
    • In vivo efficacy of combined LILRB1/PD-1 blockade not demonstrated
    • Molecular basis for LILRB1 and PD-1 expression on non-overlapping T cell subsets unknown
  14. 2020 High

    Cryo-EM/crystal structures of RIFIN–LILRB1 complexes revealed that P. falciparum RIFINs structurally mimic MHC class I to engage LILRB1 D1D2, suppressing NK perforin mobilization—the first atomic-level demonstration of pathogen molecular mimicry of an LILRB1 ligand.

    Evidence Cryo-EM/crystallography, point mutagenesis disrupting binding, reporter signaling, supported lipid bilayer NK activation assay

    PMID:32650338

    Open questions at the time
    • In vivo contribution of RIFIN–LILRB1 interaction to malaria pathogenesis not directly tested
    • Whether RIFIN engagement triggers identical downstream signaling as MHC I not confirmed
  15. 2021 High

    Discovery that RIFINs also bind LILRB1 through its D3 domain—and that LILRB1 D3D4 domain insertions into antibody genes generate RIFIN-specific antibodies in malaria-exposed individuals—revealed a second binding interface and an adaptive immune co-option mechanism.

    Evidence Cryo-EM and crystal structures of RIFIN–LILRB1 D3D4 Fab, mass spectrometry, binding assays, B cell clone isolation

    PMID:33790470

    Open questions at the time
    • Frequency and protective efficacy of LILRB1-domain-containing antibodies in endemic populations not established
    • Structural basis for simultaneous D1D2 and D3 engagement by different RIFINs not resolved
  16. 2022 Medium

    Demonstrating that LILRB1 blockade (but not LILRB2) synergizes with CD47 blockade and anti-CD20 to enhance serial macrophage phagocytosis of lymphoma cells clarified LILRB1's non-redundant role in macrophage-mediated anti-tumor immunity.

    Evidence ADCP assay with Fc-silent anti-LILRB1, lymphoma lines and primary CLL/lymphoma cells, macrophage polarization experiments

    PMID:36389667

    Open questions at the time
    • In vivo efficacy of triple blockade not tested
    • Mechanism by which LILRB1 specifically controls serial engulfment not defined
  17. 2024 High

    Identification of a LILRB1–LDLR–LDLRAP1 complex that facilitates cholesterol uptake in myeloma cells, with LILRB1 loss redirecting cells to de novo synthesis and depleting anti-ferroptotic squalene, revealed an unexpected non-immune metabolic function for LILRB1.

    Evidence Co-immunoprecipitation, LILRB1 knockout in vivo myeloma model, cholesterol uptake and squalene measurement, ferroptosis assays

    PMID:38982045

    Open questions at the time
    • Whether the LDLR complex function operates in non-malignant immune cells unknown
    • Structural basis for LILRB1–LDLR–LDLRAP1 complex assembly not determined
    • Whether ITIM signaling is involved in the metabolic function not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the full signaling cascade downstream of LILRB1 ITIM/SHP-1 to effector inhibition in each cell type; the structural and functional interplay of simultaneous D1D2 and D3D4 ligand engagement; whether the LDLR metabolic function extends to normal immune cells; and whether combined LILRB1/PD-1/CD47 blockade is efficacious in vivo.
  • Full ITIM-proximal signaling network not mapped
  • In vivo therapeutic efficacy of LILRB1 blockade combinations not established
  • Metabolic function in non-malignant contexts uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0098772 molecular function regulator activity 4
Localization
GO:0005886 plasma membrane 3
Pathway
R-HSA-168256 Immune System 6 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3
Partners
B2MHLA-FHLA-GLDLRLDLRAP1SHP-1
Complex memberships
LILRB1-LDLR-LDLRAP1

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 LILRB1 (ILT2) binds a broad range of classical and non-classical MHC class I molecules with 2- to 3-fold higher affinity than LILRB2 (ILT4), and binds HLA-G with 3- to 4-fold higher affinity than classical MHCIs; LILRB1 and LILRB2 compete with CD8 for MHC class I binding, raising the possibility that LILRB1 modulates CD8+ T cell activation by blocking CD8 binding in addition to recruiting inhibitory SHP-1 phosphatase via its ITIM motifs. Surface plasmon resonance (SPR) binding assays measuring Kd values for soluble ILT2/ILT4 vs. multiple MHC class I molecules; competition assays with CD8 Proceedings of the National Academy of Sciences of the United States of America High 12853576
2000 HLA-F directly interacts with LILRB1 (ILT2/LIR1) and LILRB2 (ILT4/LIR2); HLA-F tetramer binding to peripheral blood monocytes and B cells could be conferred on non-binding cells by transfection with ILT2 or ILT4, and a direct molecular interaction was confirmed by surface plasmon resonance. HLA-F tetramer staining, transfection of ILT2/ILT4 into non-binding cells, surface plasmon resonance European journal of immunology High 11169396
1999 LILRB1 (ILT2/CD85j) is an inhibitory MHC class I receptor of the immunoglobulin superfamily expressed on B cells, monocytes, and subsets of T and NK cells; its cell signaling role involves inhibitory functions consistent with CD85 involvement in T cell activation, as confirmed by demonstrating that anti-CD85 mAbs stain ILT2 transfectants. Affinity purification, tryptic peptide sequencing, transfectant staining with anti-CD85 mAbs Journal of leukocyte biology Medium 10380908
2002 LILRB1 (ILT2/CD85j) is functional on Sézary cell lines (CTCL): its triggering recruits SHP-1 (Src homology 2 domain-containing tyrosine phosphatase) and specifically inhibits CTCL cell proliferation induced by CD3/TCR stimulation; CD4+ILT2+ Sézary cells are less susceptible to anti-CD3-induced cell death than autologous CD4+ILT2- lymphocytes. ILT2 ligation on CTCL cell lines, SHP-1 recruitment assay, CD3/TCR stimulation proliferation assay, apoptosis comparison Blood High 12130517
2007 LILRB1 is selectively upregulated during DC differentiation from monocyte precursors; continuous ligation of LILRB1 modulates DC differentiation, confers resistance to CD95-mediated cell death, inhibits secretion of IL-10, IL-12p70, and TGF-beta, and results in poor stimulatory activity for T-cell proliferative responses that is reversed by CD80 blockade or depletion of CD4+CD25+CD127lo regulatory T cells. LILRB1 ligation during DC differentiation, cytokine ELISA, apoptosis assays, mixed lymphocyte reaction, antibody blockade experiments Blood High 18094328
2008 LILRB1 (ILT2/CD85j) inhibits IFN-gamma production by NK cells and T cells via HLA class I recognition: ligation of ILT2/CD85j with HLA class I on target cells inhibits IFN-gamma mRNA expression, protein production, and secretion in NK-92 and primary ILT2+ NK cells, and inhibits IFN-gamma in response to poly(I:C); blocking ILT2-HLA class I interactions increases IFN-gamma secretion in NK/immature DC cocultures. NK cell stimulation assays with HLA class I-expressing targets, IFN-gamma mRNA and protein measurement, ILT2 blocking antibody experiments Journal of immunology (Baltimore, Md. : 1950) High 18684926
2009 Interaction of LILRB1 (ILT2) with HLA-G inhibits polarization of NK cell lytic granules and MTOC as well as F-actin accumulation at the NK/target-cell synapse, and inhibits intracellular calcium mobilization and IFN-gamma polarized production, without affecting recruitment of activatory receptor CD2 to the synapse—demonstrating differential effects on early vs. late NK activation synapse events. NK cell/target-cell synapse imaging, granule polarization assays, MTOC localization, F-actin staining, calcium mobilization, IFN-gamma secretion assays FASEB journal : official publication of the Federation of American Societies for Experimental Biology High 19841038
2005 HLA-G upregulates expression of LILRB1 (ILT2) on antigen-presenting cells, NK cells, and T cells without requiring antigenic costimulation, suggesting that LILRB1 expression is itself regulated by its ligand HLA-G as part of an immune escape mechanism. Flow cytometry of ILT2 surface expression on immune cells after HLA-G exposure, analysis in multiple cell types FASEB journal : official publication of the Federation of American Societies for Experimental Biology Medium 15670976
2017 MHC class I (via its component β2-microglobulin) on cancer cells directly protects them from macrophage phagocytosis through the inhibitory receptor LILRB1, whose expression is upregulated on tumor-associated macrophages; disruption of either MHC class I or LILRB1 potentiates phagocytosis of tumor cells both in vitro and in vivo, defining MHC class I-LILRB1 as a phagocytosis checkpoint on macrophages. Phagocytosis assays in vitro and in vivo, LILRB1 knockdown/blockade, β2M manipulation on cancer cells, tumor-associated macrophage expression analysis Nature immunology High 29180808
2019 Crystal structure of four Ig-like domain LILRB2 and four-domain LILRB1 in complex with HLA-G1 reveals that D1D2 domains are responsible for HLA class I binding while D3D4 acts as a scaffold; the staggered assembly of four domains shows limited flexibility during ligand binding; dimeric HLA-G1 binding to LILRB1/2 suggests the dimeric receptor transduces stronger inhibitory signals. X-ray crystallography of LILRB1/2 four-domain constructs and LILRB1–HLA-G1 complex Cellular & molecular immunology High 31273318
2020 P. falciparum RIFIN proteins mimic MHC class I in their LILRB1-binding mode: cryo-EM/crystal structure of RIFIN bound to LILRB1 shows structural mimicry; a single point mutation in RIFIN disrupts the complex, blocks LILRB1 binding of all tested RIFINs, and abolishes signaling in a reporter assay; in a supported lipid bilayer system, both RIFIN and MHC are recruited to the NK cell immunological synapse and suppress NK cell perforin mobilization. Cryo-EM/crystallography of RIFIN–LILRB1 complex, mutagenesis, reporter signaling assay, supported lipid bilayer NK cell activation assay Nature High 32650338
2018 LILRB1 polymorphisms in ligand-binding domains alter functional recognition of UL18 (HCMV MHC class I homolog) and classical MHC class I but not HLA-G; N-linked glycosylation controlled by one polymorphism alters binding to all ligands tested, including enhancing binding to UL18; specific LILRB1 alleles associated with superior HCMV immune evasion are restricted by mutations that limit LILRB1 expression selectively on NK cells. LILRB1 variant expression in NK cell models, functional binding assays with UL18/classical MHCI/HLA-G, glycosylation site mutagenesis, transplant patient cohort association The Journal of clinical investigation High 29528338
2021 Crystal and cryo-EM structures of a RIFIN in complex with LILRB1 D3D4-containing antibody Fab reveal that RIFINs bind LILRB1 through its non-apical D3 domain; this interaction is similar in mode to RIFIN–LAIR1 binding; naturally occurring LILRB1 D3/D4 domain insertions in immunoglobulin VH-CH1 elbow generate RIFIN-specific antibodies in malaria-exposed donors. Cryo-EM and crystal structures of RIFIN–LILRB1 D3D4 Fab complexes, mass spectrometry, binding assays, B cell clone isolation Nature High 33790470
2016 HLA class Ia dimerization and the presence of intracellular Cys residues enhance LILRB1 recognition; type I interferon induces HLA class Ia dimer formation on primary monocytes that disproportionately increases LILRB1 interaction beyond the cytokine-induced increase in surface HLA-I expression, supporting regulated assembly of noncanonical HLA-I conformers as a mechanism to modulate LILRB1 avidity. Soluble LILRB1-Fc fusion protein binding, LILRB1-ζ chimera cellular reporter system, HLA-I transfectants in 721.221 cells, IFN treatment of primary monocytes European journal of immunology Medium 27109306
2019 LILRB1 functions as a negative regulator of human CD45RA+CCR7- CD8+ effector T cells; LILRB1 is expressed on distinct CD8+ T cell populations from PD1; engaging LILRB1 with HLA-G on tumor cells significantly inhibited BiTE molecule-induced CD8+ T cell activation; combined blockade of LILRB1 and PD1 induced greater CD8+ T cell activation than either alone. Flow cytometry of CD8+ T cell subsets, BiTE molecule stimulation assays, HLA-G engagement assays, dual blockade experiments Journal of immunology (Baltimore, Md. : 1950) Medium 31253728
2024 LILRB1 forms a complex with the low-density lipoprotein receptor (LDLR) and LDLR adapter protein 1 (LDLRAP1) to facilitate LDL/cholesterol uptake in multiple myeloma cells; loss of LILRB1 impairs cholesterol uptake but activates de novo cholesterol synthesis, decreasing the anti-ferroptotic metabolite squalene and thereby enhancing ferroptosis of myeloma cells. Co-immunoprecipitation of LILRB1-LDLR-LDLRAP1 complex, LILRB1 knockout in vivo myeloma model, cholesterol uptake assays, squalene measurement, ferroptosis assays Nature communications High 38982045
2020 LILRB1 blockade on NK cells increases tumoricidal activity against multiple myeloma, leukemia, lymphoma and solid tumor cells both in vitro and in vivo, and the percentage of LILRB1+ NK cells is significantly higher in patients with persistent multiple myeloma or late-stage prostate cancer than in healthy donors. Antagonistic anti-LILRB1 monoclonal antibody treatment, in vitro cytotoxicity assays, NOD-SCID IL-2Rγ-null mouse xenograft model, flow cytometry of NK cells from cancer patients Journal for immunotherapy of cancer Medium 32771992
2022 Dual blockade of CD47 and LILRB1 significantly enhances antibody-dependent cellular phagocytosis (ADCP) of lymphoma cell lines and primary CLL/lymphoma cells by macrophages when combined with rituximab; LILRB1 blockade (but not LILRB2 blockade) promotes serial engulfment and potentiates ADCP by M0, M1, and M2 macrophages, but requires CD47 co-blockade and presence of CD20 antibody. ADCP phagocytosis assay with Fc-silent anti-LILRB1 antibody, lymphoma cell lines and primary patient cells, macrophage polarization experiments Frontiers in immunology Medium 36389667
2019 CD8+ILT2+ tumor-infiltrating lymphocytes (TILs) are a late-differentiated cytotoxic CD27-CD28-CD57+ subset distinct from CD8+PD-1+ TILs; HLA-G expression on target cells specifically inhibits CD8+ILT2+ T cell cytotoxicity and IFNγ production, but not CD8+ILT2- or CD8+PD-1+ counterparts; blockade of HLA-G/ILT2 interaction restores cytotoxicity. Ex vivo flow cytometry, functional cytotoxicity assays with TILs and PBMCs, HLA-G blocking antibody experiments Cancer immunology research Medium 31451484

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 CircHIPK3 promotes colorectal cancer growth and metastasis by sponging miR-7. Cell death & disease 500 29549306
2017 Engagement of MHC class I by the inhibitory receptor LILRB1 suppresses macrophages and is a target of cancer immunotherapy. Nature immunology 473 29180808
2003 Human inhibitory receptors Ig-like transcript 2 (ILT2) and ILT4 compete with CD8 for MHC class I binding and bind preferentially to HLA-G. Proceedings of the National Academy of Sciences of the United States of America 447 12853576
2005 HLA-G up-regulates ILT2, ILT3, ILT4, and KIR2DL4 in antigen presenting cells, NK cells, and T cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 244 15670976
2019 ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2. Journal of experimental & clinical cancer research : CR 201 30987661
2000 Functional characterization of HLA-F and binding of HLA-F tetramers to ILT2 and ILT4 receptors. European journal of immunology 159 11169396
2013 Tissue-specific control of brain-enriched miR-7 biogenesis. Genes & development 132 23307866
2019 MiR-7-5p suppresses tumor metastasis of non-small cell lung cancer by targeting NOVA2. Cellular & molecular biology letters 126 31832068
2008 MicroRNA miR-7 is preferentially expressed in endocrine cells of the developing and adult human pancreas. Gene expression patterns : GEP 125 19135553
2014 miR-7 inhibits glioblastoma growth by simultaneously interfering with the PI3K/ATK and Raf/MEK/ERK pathways. International journal of oncology 118 24603851
2007 Quantitative differential expression analysis reveals miR-7 as major islet microRNA. Biochemical and biophysical research communications 118 18086561
2009 ILT2/HLA-G interaction impairs NK-cell functions through the inhibition of the late but not the early events of the NK-cell activating synapse. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 103 19841038
2018 The CDR1as/miR-7/TGFBR2 Axis Modulates EMT in Silica-Induced Pulmonary Fibrosis. Toxicological sciences : an official journal of the Society of Toxicology 98 30202956
2021 METTL14 promotes doxorubicin-induced cardiomyocyte ferroptosis by regulating the KCNQ1OT1-miR-7-5p-TFRC axis. Cell biology and toxicology 94 34648132
2019 Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway. Journal of cellular and molecular medicine 88 31821687
2007 The inhibitory receptor LILRB1 modulates the differentiation and regulatory potential of human dendritic cells. Blood 84 18094328
2013 Identification of miR-7 as an oncogene in renal cell carcinoma. Journal of molecular histology 78 23793934
2012 Expression of immunoglobulin-like transcript (ILT)2 and ILT3 in human gastric cancer and its clinical significance. Molecular medicine reports 77 22246571
2018 miR-7 Replacement Therapy in Parkinson's Disease. Current gene therapy 74 29714132
2019 Inhibition of circular RNA CDR1as increases chemosensitivity of 5-FU-resistant BC cells through up-regulating miR-7. Journal of cellular and molecular medicine 69 30884120
2018 Long non-coding RNA KCNQ1OT1 modulates oxaliplatin resistance in hepatocellular carcinoma through miR-7-5p/ ABCC1 axis. Biochemical and biophysical research communications 69 29966655
2015 miR-7 modulates chemoresistance of small cell lung cancer by repressing MRP1/ABCC1. International journal of experimental pathology 68 26108539
2004 Immunoglobulin-like transcripts ILT2, ILT3 and ILT7 are expressed by human dendritic cells and down-regulated following activation. Gene 67 15094202
2020 Long non-coding RNA LPP-AS2 promotes glioma tumorigenesis via miR-7-5p/EGFR/PI3K/AKT/c-MYC feedback loop. Journal of experimental & clinical cancer research : CR 66 32962742
2019 CD8+PD-1-ILT2+ T Cells Are an Intratumoral Cytotoxic Population Selectively Inhibited by the Immune-Checkpoint HLA-G. Cancer immunology research 62 31451484
2019 Dihydroartemisinin inhibits prostate cancer via JARID2/miR-7/miR-34a-dependent downregulation of Axl. Oncogenesis 59 30783079
2022 lncRNA ZFAS1 Positively Facilitates Endothelial Ferroptosis via miR-7-5p/ACSL4 Axis in Diabetic Retinopathy. Oxidative medicine and cellular longevity 56 36092160
1999 Identification of the CD85 antigen as ILT2, an inhibitory MHC class I receptor of the immunoglobulin superfamily. Journal of leukocyte biology 56 10380908
2017 Exosomal miR-7 Mediates Bystander Autophagy in Lung after Focal Brain Irradiation in Mice. International journal of biological sciences 55 29104495
2017 DNA Methylation of miR-7 is a Mechanism Involved in Platinum Response through MAFG Overexpression in Cancer Cells. Theranostics 52 29158814
2014 MiR-7 promotes epithelial cell transformation by targeting the tumor suppressor KLF4. PloS one 52 25181544
2019 The MHC class I-LILRB1 signalling axis as a promising target in cancer therapy. Scandinavian journal of immunology 51 31267559
2020 Antagonistic anti-LILRB1 monoclonal antibody regulates antitumor functions of natural killer cells. Journal for immunotherapy of cancer 50 32771992
2019 HIV-1 Tat-Induced Astrocytic Extracellular Vesicle miR-7 Impairs Synaptic Architecture. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology 49 31401755
2019 Long noncoding RNA SOX21-AS1 promotes cervical cancer progression by competitively sponging miR-7/VDAC1. Journal of cellular physiology 47 30912129
2021 MiR-7 in Cancer Development. Biomedicines 46 33806891
2017 Cancer-associated fibroblasts promote cancer cell growth through a miR-7-RASSF2-PAR-4 axis in the tumor microenvironment. Oncotarget 46 27901488
2021 Exosomes-transmitted miR-7 reverses gefitinib resistance by targeting YAP in non-small-cell lung cancer. Pharmacological research 45 33497805
2020 Structural basis for RIFIN-mediated activation of LILRB1 in malaria. Nature 43 32650338
2019 Structures of the four Ig-like domain LILRB2 and the four-domain LILRB1 and HLA-G1 complex. Cellular & molecular immunology 43 31273318
2019 miR-7 Reverses Breast Cancer Resistance To Chemotherapy By Targeting MRP1 And BCL2. OncoTargets and therapy 43 31908478
2012 Impact of miR-7 over-expression on the proteome of Chinese hamster ovary cells. Journal of biotechnology 42 22445466
2022 Exosome-mediated miR-7-5p delivery enhances the anticancer effect of Everolimus via blocking MNK/eIF4E axis in non-small cell lung cancer. Cell death & disease 41 35136028
2020 Combinatory Treatment with miR-7-5p and Drug-Loaded Cubosomes Effectively Impairs Cancer Cells. International journal of molecular sciences 41 32708846
2019 LILRB1 Blockade Enhances Bispecific T Cell Engager Antibody-Induced Tumor Cell Killing by Effector CD8+ T Cells. Journal of immunology (Baltimore, Md. : 1950) 41 31253728
2019 Curcumin Prevents Brain Damage and Cognitive Dysfunction During Ischemic-reperfusion Through the Regulation of miR-7-5p. Current neurovascular research 41 31660818
2018 Ig-Like Transcript 2 (ILT2) Blockade and Lenalidomide Restore NK Cell Function in Chronic Lymphocytic Leukemia. Frontiers in immunology 41 30619281
2022 CDR1as regulates α-synuclein-mediated ischemic brain damage by controlling miR-7 availability. Molecular therapy. Nucleic acids 40 36618263
2008 HLA class I molecules regulate IFN-gamma production induced in NK cells by target cells, viral products, or immature dendritic cells through the inhibitory receptor ILT2/CD85j. Journal of immunology (Baltimore, Md. : 1950) 40 18684926
2022 BND-22, a first-in-class humanized ILT2-blocking antibody, promotes antitumor immunity and tumor regression. Journal for immunotherapy of cancer 39 36096532
2022 Dual checkpoint blockade of CD47 and LILRB1 enhances CD20 antibody-dependent phagocytosis of lymphoma cells by macrophages. Frontiers in immunology 37 36389667
2021 Propofol suppresses lung cancer tumorigenesis by modulating the circ-ERBB2/miR-7-5p/FOXM1 axis. Thoracic cancer 37 33506582
2018 miR-7-5p acts as a tumor suppressor in bladder cancer by regulating the hedgehog pathway factor Gli3. Biochemical and biophysical research communications 36 30100065
2008 Rapamycin downregulates the inhibitory receptors ILT2, ILT3, ILT4 on human dendritic cells and yet induces T cell hyporesponsiveness independent of FoxP3 induction. Immunology letters 36 18652845
2023 Perspectives of targeting LILRB1 in innate and adaptive immune checkpoint therapy of cancer. Frontiers in immunology 34 37781391
2020 lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 34 32353178
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