Affinage

CD160

CD160 antigen · UniProt O95971

Length
181 aa
Mass
19.8 kDa
Annotated
2026-06-09
100 papers in source corpus 20 papers cited in narrative 20 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

CD160 is an immunoglobulin-superfamily receptor expressed on cytotoxic NK cells (CD56dim/CD16+), CD8+CD28- T cell subsets, and intestinal intraepithelial lymphocytes that delivers context-dependent activating or inhibitory signals to control lymphocyte effector function (PMID:9743336). It was originally characterized as a cysteine-rich, GPI-anchored protein forming tightly disulfide-linked multimers (PMID:9743336), with a later-discovered alternatively spliced transmembrane isoform (CD160-TM) restricted to activated NK cells (PMID:19109136). On NK cells, CD160 engages MHC class I (HLA-C) and HVEM to trigger cytotoxicity and inflammatory cytokine production through a Syk–PI3K–AKT–ERK signaling cascade, with the CD160-TM cytoplasmic tail signaling via the Src-family kinase p56lck (PMID:12486241, PMID:17307798, PMID:19109136, PMID:23761635); this pathway is selectively required for NK-cell IFN-γ production rather than cytotoxicity, as shown in CD160-deficient mice that lose control of NK-sensitive tumors (PMID:25711213). The same PI3K-dependent survival program is co-opted in chronic lymphocytic leukemia cells, where CD160 activation upregulates Bcl-2/Bcl-xL/Mcl-1 and protects against apoptosis (PMID:20164468). On T cells and NKT cells, CD160 engagement of HVEM at its CRD1 surface delivers a coinhibitory signal that dampens TCR-driven activation and innate cytokine output (PMID:18193050, PMID:31332204), while the receptor also acts as a costimulator of TCR-redirected killing in differentiated CD8+ effector cells (PMID:11978774, PMID:16917959). Crystallography established that CD160 is a monomeric Ig fold binding HVEM in a 1:1 complex distinct from the LIGHT-binding site, and that HVEM can simultaneously engage LIGHT and CD160 in a ternary complex, providing the structural basis for bidirectional immune regulation (PMID:31230945, PMID:34709351). CD160 is additionally expressed selectively on tumor-associated neovascular endothelium, where antibody targeting causes regression of tumor vasculature (PMID:21482699).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 High

    Established CD160 as a distinct molecular entity by cloning it and showing it is a GPI-anchored, multimeric cysteine-rich Ig-like protein with lymphocyte-restricted expression.

    Evidence cDNA cloning, reducing/non-reducing immunoprecipitation, RNA blot, and flow cytometry on NK and T cell subsets

    PMID:9743336

    Open questions at the time
    • No ligand or signaling function defined at this stage
    • Multimerization stoichiometry of the native receptor not resolved
  2. 2002 High

    Identified MHC class I (HLA-C) as a CD160 ligand whose engagement triggers NK cytolysis, defining CD160 as a functional activating receptor.

    Evidence Recombinant soluble HLA-Cw3/CD160 binding plus antibody-blocking cytotoxicity assays

    PMID:12486241

    Open questions at the time
    • Downstream signaling cascade not yet mapped
    • Affinity and physiological relevance of HLA-C binding versus other ligands not quantified
  3. 2002 Medium

    Showed CD160 functions as a TCR co-receptor on CD28-negative CD8+ effector T cells, physically linking it to proximal TCR signaling machinery.

    Evidence Anti-CD160 proliferation assays and co-immunoprecipitation with p56lck and phospho-zeta chains

    PMID:11978774

    Open questions at the time
    • GPI-anchored isoform lacks a cytoplasmic tail, leaving the mechanism of p56lck coupling unexplained
    • Single-lab co-IP without reciprocal validation
  4. 2007 High

    Defined the NK-cell signaling cascade downstream of CD160 as Syk→PI3K→AKT/ERK, explaining how engagement drives both cytotoxicity and cytokine release.

    Evidence Pharmacological inhibitors of PI3K/MEK/Syk, confocal co-localization, and phospho-Western blotting in primary human NK cells

    PMID:17307798

    Open questions at the time
    • How a GPI-anchored receptor recruits Syk/PI3K not resolved
    • Inhibitor specificity caveats for the kinase assignments
  5. 2008 High

    Identified HVEM as a second CD160 ligand and reversed the functional picture by showing CD160-HVEM engagement coinhibits T cell activation via the HVEM CRD1 domain.

    Evidence HVEM CRD1 deletion mutagenesis with T cell activation/cytokine assays and HVEM-transfected co-culture

    PMID:18193050

    Open questions at the time
    • Relative contributions of CD160 versus BTLA at shared CRD1 surface not separated
    • Inhibitory signaling output of CD160 not mechanistically traced
  6. 2009 Medium

    Discovered the transmembrane isoform CD160-TM and showed its cytoplasmic tail is sufficient for p56lck-dependent ERK signaling and NK degranulation, providing a signaling-competent form of the receptor.

    Evidence RT-PCR isoform characterization, Src-kinase inhibitor experiments, CD107a mobilization assays

    PMID:19109136

    Open questions at the time
    • Relative physiological abundance of TM versus GPI isoform unclear
    • Direct kinase-tail interaction not biochemically demonstrated
  7. 2010 High

    Demonstrated that CD160-PI3K signaling drives a pro-survival program in CLL cells, extending the activating cascade to a pathological context.

    Evidence CLL cell culture with CD160 stimulation, Bcl-2 family Westerns, apoptosis/proliferation assays, PI3K inhibition

    PMID:20164468

    Open questions at the time
    • Ligand driving CD160 activation in CLL not identified
    • Connection to the NK Syk–PI3K cascade not formally established
  8. 2013 High

    Established that HVEM, not other shared ligands, costimulates CD160 on NK cells to enhance cytolysis and cytokine output, contrasting with HVEM-BTLA inhibition.

    Evidence NK activation assays, phospho-ERK/AKT Westerns, cytotoxicity and cytokine ELISAs with BTLA as comparator

    PMID:23761635

    Open questions at the time
    • How identical HVEM engagement yields opposite outcomes on NK (activating) versus T cells (inhibitory) not resolved
  9. 2012 Medium

    Linked CD160 to T cell exhaustion, showing CD160/PD-1 co-expression marks dysfunctional HIV-specific CD8 T cells and that CD160/HVEM blockade restores function.

    Evidence Flow phenotyping, HVEM-blocking functional assays, transcriptional profiling of exhausted T cells

    PMID:22916009

    Open questions at the time
    • Whether CD160 acts via HVEM exclusively in exhaustion not isolated
    • Correlation versus causation in the exhaustion signature
  10. 2014 Medium

    Resolved that CD160-mediated CD8 T cell suppression operates independently of PD-1 and is not activation-induced, distinguishing it from the canonical exhaustion checkpoint.

    Evidence Anti-CD160 blocking with proliferation/perforin readouts across influenza/EBV/CMV-specific T cells

    PMID:25255144

    Open questions at the time
    • The CD160 ligand operative in these settings not pinned down
    • Correlative restoration data
  11. 2014 Medium

    Showed both CD160 isoforms bind HVEM with differing efficiency and that CD160-GPI triggering can deliver a positive costimulatory signal, underscoring the receptor's bidirectional output.

    Evidence Time-resolved fluorescence binding, Jurkat activation assays, antibody-blocking and HIV-antigen PBMC stimulation

    PMID:25179432

    Open questions at the time
    • Molecular basis for isoform-dependent HVEM binding differences unresolved
    • Single-lab functional assays
  12. 2015 High

    Used genetic knockout to dissociate CD160 functions, proving it is intrinsically required for NK-cell IFN-γ production but dispensable for cytotoxicity in tumor control.

    Evidence CD160-/- mice, tumor challenge, bone marrow chimeras, soluble CD160-Ig decoy, intratumoral NK transfer

    PMID:25711213

    Open questions at the time
    • Ligand driving the in vivo NK IFN-γ response not defined
    • Reconciliation with earlier reports of CD160-driven cytotoxicity
  13. 2018 High

    Demonstrated a cell-intrinsic costimulatory role for CD160 on CD8 T cells and IELs during oral Listeria infection, revealing a protective effector function in vivo.

    Evidence CD160-/- infection model, granzyme B/IFN-γ/TNF flow cytometry, RAG-/- adoptive transfer

    PMID:31022694

    Open questions at the time
    • Costimulatory versus coinhibitory role context-dependence not mechanistically explained
    • Ligand engaged during mucosal infection unidentified
  14. 2019 High

    Established CD160 as a non-redundant coinhibitory receptor on NKT cells that limits innate cytokine-driven liver injury, parallel to but distinct from BTLA.

    Evidence CD160-/- mice, mixed bone marrow chimeras, α-GalCer/ConA challenge, anti-BTLA dissection

    PMID:31332204

    Open questions at the time
    • Inhibitory signaling mechanism in NKT cells not traced
    • How CD160 and BTLA divide labor at shared HVEM not resolved
  15. 2019 High

    Provided the atomic-level basis for CD160-HVEM recognition, showing CD160 is a monomeric Ig fold binding HVEM 1:1 at an interface resembling BTLA:HVEM.

    Evidence X-ray crystallography of CD160 alone and the CD160:HVEM complex

    PMID:31230945

    Open questions at the time
    • Reconciliation of monomeric solution behavior with earlier disulfide-multimer biochemistry
    • Structure does not explain divergent signaling outputs
  16. 2021 High

    Defined how HVEM coordinates competing ligands, showing distinct surfaces for LIGHT versus CD160/BTLA, a ternary LIGHT-HVEM-CD160 complex, and selective in vivo functions of each axis.

    Evidence Crystal structures (HVEM, HVEM-LIGHT, HVEM-CD160, ternary) plus HVEM ligand-selective knockin mice in infection/inflammation models

    PMID:34709351

    Open questions at the time
    • Functional consequence of simultaneous LIGHT/CD160 occupancy on the same HVEM not directly tested
    • Whether ternary complex forms physiologically in tissue
  17. 2018 Medium

    Linked CD160+ NK cells to a high-IFN-γ functional program suppressed by TGFβ1, identifying a microenvironmental brake on CD160-driven NK activation.

    Evidence Sorted CD160+/- NK transcriptomics, GSEA, and TGFβ1-blocking IFN-γ rescue

    PMID:30232222

    Open questions at the time
    • Mechanism of TGFβ1 interference with CD160 signaling not defined
    • Correlative transcriptomics
  18. 2011 Medium

    Revealed a non-lymphocyte role for CD160 as a marker of tumor neovascular endothelium and a therapeutic anti-angiogenic target.

    Evidence Immunohistochemistry and anti-CD160 antibody across rabbit cornea, retinopathy, Matrigel, and melanoma models

    PMID:21482699

    Open questions at the time
    • Endothelial CD160 ligand and signaling mechanism unknown
    • Relationship to lymphocyte CD160 function unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single receptor delivers opposite (activating versus inhibitory) signals depending on cell type and ligand, and how GPI-anchored CD160 lacking a cytoplasmic tail couples to intracellular kinases.
  • No structural or biochemical mechanism for GPI-isoform signal transduction
  • No unified model reconciling costimulatory and coinhibitory outcomes
  • Ligand(s) governing each functional context not fully mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3
Partners
BTLAHLA-CHVEMLCKLIGHT

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 CD160 (BY55) is a GPI-anchored, cysteine-rich protein of 181 amino acids with a single Ig-like domain weakly homologous to killer inhibitory receptors. Reduction and carboxyamidomethylation of immunoprecipitated BY55 gave a 27 kDa band, whereas reduction alone gave 80 kDa, indicating CD160 forms tightly disulfide-linked multimers. Expression is restricted to CD56dim/CD16+ NK cells (high cytolytic activity) but not CD56bright/CD16- NK cells, and to CD8+CD28- T cells and intestinal intraepithelial lymphocytes. cDNA cloning, immunoprecipitation with reducing/non-reducing SDS-PAGE, RNA blot analysis, flow cytometry Journal of immunology High 9743336
2002 CD160 receptor engagement by HLA-C molecules (constitutively expressed on K562 cells) triggers NK cell cytolytic activity. Direct interaction between recombinant soluble HLA-Cw3 and CD160 proteins was demonstrated. CD158b inhibitory receptors partially interfere with CD160-mediated cytotoxicity, whereas CD94/CD159a and CD85j do not. Monoclonal antibody blocking assays, cytotoxicity assays, recombinant protein binding (soluble HLA-Cw3 and CD160), flow cytometry Proceedings of the National Academy of Sciences of the United States of America High 12486241
2002 CD160 acts as a co-receptor in TCR signal transduction on CD28-negative cytotoxic effector CD8+ T cells. Anti-CD160 mAb enhances CD3-induced proliferation, and CD160 co-precipitates with protein tyrosine kinase p56lck and tyrosine-phosphorylated zeta chains upon TCR-CD3 activation. Anti-CD160 mAb stimulation, proliferation assays, co-immunoprecipitation (CD160 with p56lck and phospho-zeta chains) International immunology Medium 11978774
2007 CD160-mediated NK cell effector functions (cytotoxicity and cytokine production: IFN-γ, TNF-α, IL-6) require phosphatidylinositol 3-kinase (PI3K) signaling. CD160 engagement induces PI3K polarization and co-localization with CD160, Akt phosphorylation, and ERK phosphorylation. Syk kinase acts upstream of PI3K in this cascade. PI3K inhibitors abrogate both CD160-mediated cytotoxicity and cytokine release; MEK inhibitors block cytokine release; Syk inhibitors block cytokine release. Confocal microscopy, pharmacological inhibitors of PI3K/MEK/Syk, Western blotting (phospho-Akt), freshly isolated human NK cells International immunology High 17307798
2008 CD160 inhibits human CD4+ T cell activation through interaction with HVEM (herpesvirus entry mediator). Crosslinking CD160 strongly inhibits CD3/CD28-mediated activation. HVEM CRD1 (cysteine-rich domain 1) is required for CD160 binding; deletion of CRD1 abolishes CD160 and BTLA binding but not LIGHT binding, converting HVEM into a dominant costimulatory molecule. Inhibition of CD4+ T cell activation by HVEM-transfected cells is dependent on both CD160 and BTLA. Monoclonal antibody crosslinking, T cell activation assays, HVEM deletion mutants (CRD1 deletion), HVEM-transfected cell co-culture, cytokine/proliferation readouts Nature immunology High 18193050
2009 CD160 has a transmembrane isoform (CD160-TM) generated by alternative splicing. CD160-TM surface expression is highly restricted to NK cells and is activation-dependent. The CD160-TM cytoplasmic tail is sufficient to mediate ERK1/2 signaling, and initiation of this activation is dependent on the Src-family kinase p56lck. CD160-TM engagement increases CD107a mobilization (degranulation marker). Alternative splicing characterization by RT-PCR, flow cytometry, NK cell activation assays (CD107a mobilization), Src kinase inhibitor experiments, ERK1/2 signaling readouts Journal of immunology Medium 19109136
2010 CD160 signaling in CLL cells activates PI3K-dependent survival and growth signals. CD160 activation protects CLL cells from spontaneous apoptosis, upregulates Bcl-2, Bcl-xL, and Mcl-1, reduces mitochondrial membrane potential collapse and cytochrome c release, induces DNA synthesis and proliferation, and stimulates secretion of IL-6 and IL-8. PI3K inhibitors suppress these survival and activation signals in a dose-dependent manner. In vitro CLL cell culture with CD160 stimulation, cell viability assays, Western blotting (Bcl-2 family proteins), mitochondrial membrane potential assays, cytochrome c release assays, DNA synthesis/proliferation assays, ELISA (IL-6, IL-8), PI3K pharmacological inhibitors Blood High 20164468
2011 CD160 is expressed on endothelial cells of newly formed blood vessels in human colon carcinoma and mouse melanoma, but not on vessels of healthy tissues. Monoclonal antibody CL1-R2 targeting CD160 reduces FGF2-induced neovascularization in rabbit cornea, oxygen-induced retinopathy, and Matrigel plug assays. In tumor-bearing mice, anti-CD160 combined with cyclophosphamide caused tumor vasculature regression and normalization of remaining vessels. Immunohistochemistry, in vivo models (rabbit cornea, retinopathy, Matrigel plug, B16 melanoma), Doppler ultrasonography, intravital microscopy, histology The Journal of experimental medicine Medium 21482699
2012 CD160 and PD-1 co-expression on HIV-specific CD8 T cells defines a functionally exhausted subset. Blocking CD160/HVEM interaction increased HIV-specific CD8 T cell proliferation and cytokine production. Transcriptional profiling showed CD160+PD-1+ T cells have downregulation of the NFκB transcriptional node and upregulation of inhibitors of T cell survival and function. Flow cytometry phenotyping, HVEM-blocking antibody functional assays (proliferation, cytokine production), transcriptional profiling PLoS pathogens Medium 22916009
2013 HVEM activates CD160 on effector NK cells to enhance inflammatory cytokine production and cytolysis. Human CD56dim NK cells are costimulated specifically by HVEM but not by other receptors sharing HVEM ligands (LIGHT, LTα, BTLA). Tumor cell-expressed HVEM activates CD160 in NK cells, causing rapid hyperphosphorylation of ERK1/2 and AKT and enhanced target cell cytolysis. In contrast, HVEM activation of BTLA reduces cytolysis. Human NK cell activation assays, cytokine ELISA (IFN-γ, TNF-α), Western blotting (phospho-ERK1/2, phospho-AKT), cytotoxicity assays, NK cell line experiments Journal of immunology High 23761635
2014 CD160-associated CD8 T cell functional impairment (reduced proliferation and perforin expression) is independent of PD-1 expression. Blockade of CD160/CD160-ligand interaction restores CD8 T cell proliferation capacity in a manner that correlates with the proportion of CD160+ CD8 T cells, indicating CD160 negatively regulates TCR-mediated signaling. CD160 expression was not upregulated upon T cell activation or proliferation, unlike PD-1. Flow cytometry, anti-CD160 blocking antibody, proliferation assays, perforin expression analysis, virus-specific CD8 T cell functional assays (influenza, EBV, CMV) PLoS pathogens Medium 25255144
2014 Both CD160 isoforms (CD160-GPI and CD160-TM) are expressed in human primary CD4+ and CD8+ T cells and are recognized by HVEM ligand, though binding is less pronounced with CD160-TM. HVEM-specific antibodies block HVEM binding to CD160-GPI but enhance HVEM binding to CD160-TM (suggesting antibody-mediated HVEM multimerization or conformational changes facilitate CD160-TM binding). Triggering CD160-GPI on Jurkat cells with bead-bound HVEM-Fc or anti-CD160 mAb enhances cell activation (positive costimulatory role). CD160-GPI-specific antibodies combined with PD-1 blockade synergistically enhance HIV-specific CD8+ T cell proliferation. Quantitative RT-PCR, flow cytometry, Time-Resolved Fluorescence binding assay, Jurkat cell activation assays, ex vivo PBMC stimulation with HIV antigens, antibody blocking experiments Journal of translational medicine Medium 25179432
2015 CD160 is essential for NK cell IFN-γ production but not cytotoxicity. CD160-deficient mice show severely compromised control of NK-sensitive tumors due to markedly reduced IFN-γ secretion by NK cells (not impaired cytotoxicity). A soluble CD160-Ig fusion protein impairs tumor control and IFN-γ production. Reciprocal bone marrow transfer identifies the intrinsic role of CD160 on NK cells. Intratumoral transfer of CD160+ NK fraction into CD160-/- tumor-bearing mice causes tumor regression. CD160 knockout mouse generation, tumor challenge assays, IFN-γ ELISA/intracellular cytokine staining, cytotoxicity assays, soluble CD160-Ig fusion protein treatment, reciprocal bone marrow transfer, intratumoral cell transfer The Journal of experimental medicine High 25711213
2018 CD160 provides costimulatory signals to CD8+ T cells required for optimal effector functions during oral Listeria monocytogenes infection. CD160-/- mice fail to clear oral L. monocytogenes efficiently; this defect is attributable to compromised CD8+ T cells and intraepithelial lymphocytes (not NK cells). CD160-/- CD8+ T cells show reduced granzyme B expression and IFN-γ/TNF-α co-production. Adoptive transfer of CD160-/- CD8+ T cells into RAG-/- recipients results in higher mortality, weight loss, and bacterial burden compared to WT CD8+ T cells. CD160 knockout mice, in vivo infection model, flow cytometry (granzyme B, IFN-γ, TNF-α), RAG-/- reconstitution experiments, adoptive transfer ImmunoHorizons High 31022694
2019 CD160 serves as a co-inhibitory receptor on NKT cells that dampens cytokine production during early innate immune activation. CD160-/- mice develop severe liver injury after α-galactosylceramide or Concanavalin A challenge, with hyperactivation of NKT cells, elevated AST/ALT, and enhanced IFN-γ, TNF, and IL-4 production. Mixed bone marrow chimeras show this is NKT cell-intrinsic. CD160 and BTLA serve as non-overlapping negative regulators of NKT cells (anti-BTLA mAb aggravates injury in CD160-/- mice). CD160 knockout mice, mixed bone marrow chimeras, in vivo α-GalCer and ConA challenge, serum ALT/AST measurement, intracellular cytokine staining, anti-BTLA antibody treatment Nature communications High 31332204
2019 Crystal structure of the human CD160 extracellular domain and its complex with human HVEM was determined. CD160 adopts a unique variation of the immunoglobulin fold and exists as a monomer in solution. The CD160:HVEM assembly shows 1:1 stoichiometry with a binding interface similar to the BTLA:HVEM complex, revealing the chemical and physical determinants of CD160-HVEM recognition. X-ray crystallography (crystal structure of CD160 alone and CD160:HVEM complex) Structure High 31230945
2021 Crystal structures of HVEM revealed distinct surfaces that engage LIGHT (TNF ligand) versus BTLA/CD160 (Ig superfamily ligands), including a human HVEM-LIGHT-CD160 ternary complex showing HVEM can interact simultaneously with both LIGHT and CD160. HVEM knockin mutants that selectively recognize either TNF or Ig ligands in mice demonstrate selective functions: LIGHT binding mediates bacterial clearance in the intestine; Ig ligand (BTLA/CD160) binding ameliorates liver inflammation. X-ray crystallography (HVEM alone, HVEM-LIGHT, HVEM-CD160, ternary complex), generation of HVEM knockin mutant mice, in vivo infection/inflammation models The Journal of experimental medicine High 34709351
2006 CD160 does not independently induce cytotoxicity but costimulates CD3-redirected killing in 2B4+CD160+ CD8+ T cells. The 2B4+CD160+ subset expresses high amounts of perforin and granzyme B, and CD160 expression increases from naive to terminally differentiated phenotype during CTL ontogeny. Flow cytometry, intracellular perforin/granzyme B staining, CD3-redirected cytotoxicity assays with anti-CD160 mAb, phenotypic analysis of CTL subsets European journal of immunology Medium 16917959
2007 CD160 acts as a co-activator receptor for CD3-induced proliferation of CD4+CD160+ T cells isolated from inflammatory skin lesions. A novel CD4+CD160+ T cell subset was identified infiltrating inflammatory skin lesions (atopic dermatitis, contact dermatitis, psoriasis). CD160 transcripts can be induced in IL-2 or IL-15-activated CD4+ peripheral blood lymphocytes. Immunohistochemistry, CD3-induced proliferation assays with anti-CD160 mAb costimulation, RT-PCR, flow cytometry The Journal of investigative dermatology Low 17218942
2018 TGFβ1 interferes with IFN-γ production by CD160+ NK cells; blocking TGFβ1 restores IFN-γ production specifically in CD160+ NK cells to normal levels. Transcriptomic analysis of sorted CD160+ and CD160- NK cells revealed that CD160+ NK cells have functional activation and high IFN-γ production programs. Flow cytometry sorting of CD160+ and CD160- NK cells, gene set enrichment analysis/microarray, TGFβ1 blocking antibody, IFN-γ ELISA Cancer research Medium 30232222

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Mouse CD1-specific NK1 T cells: development, specificity, and function. Annual review of immunology 986 9143699
2008 CD160 inhibits activation of human CD4+ T cells through interaction with herpesvirus entry mediator. Nature immunology 283 18193050
2002 A natural killer T (NKT) cell developmental pathway iInvolving a thymus-dependent NK1.1(-)CD4(+) CD1d-dependent precursor stage. The Journal of experimental medicine 282 11927628
1995 Mouse NK1+ T cells. Current opinion in immunology 256 7546402
1998 The tachykinin NK1 receptor. Part II: Distribution and pathophysiological roles. Neuropeptides 248 9571643
2009 The CD160, BTLA, LIGHT/HVEM pathway: a bidirectional switch regulating T-cell activation. Immunological reviews 247 19426226
2009 CCR6 and NK1.1 distinguish between IL-17A and IFN-gamma-producing gammadelta effector T cells. European journal of immunology 236 19830744
1999 Bone marrow NK1.1(-) and NK1.1(+) T cells reciprocally regulate acute graft versus host disease. The Journal of experimental medicine 232 10190898
1999 Discovery of the antidepressant and anti-emetic efficacy of substance P receptor (NK1) antagonists. Trends in pharmacological sciences 222 10671176
1998 Differentiation of human NK cells into NK1 and NK2 subsets. Journal of immunology (Baltimore, Md. : 1950) 222 9834059
2002 Neurobiology of substance P and the NK1 receptor. The Journal of clinical psychiatry 221 12562137
1996 Mouse NK1.1+ T cells: a new family of T cells. Immunology today 213 8808053
1995 Delineation of the endocytic pathway of substance P and its seven-transmembrane domain NK1 receptor. Molecular biology of the cell 196 7545030
1999 The tachykinin NK1 receptor in the brain: pharmacology and putative functions. European journal of pharmacology 176 10443564
1997 The tachykinin NK1 receptor. Part I: ligands and mechanisms of cellular activation. Neuropeptides 174 9574822
2015 Biological and Pharmacological Aspects of the NK1-Receptor. BioMed research international 162 26421291
2014 Involvement of substance P and the NK-1 receptor in human pathology. Amino acids 158 24705689
2009 HVEM/LIGHT/BTLA/CD160 cosignaling pathways as targets for immune regulation. Journal of leukocyte biology 133 20007250
2007 Development and function of murine B220+CD11c+NK1.1+ cells identify them as a subset of NK cells. The Journal of experimental medicine 131 17923504
2012 CD160 and PD-1 co-expression on HIV-specific CD8 T cells defines a subset with advanced dysfunction. PLoS pathogens 124 22916009
2005 Role of NK-1 neurotransmission in opioid-induced hyperalgesia. Pain 122 15964684
2013 Involvement of substance P and the NK-1 receptor in cancer progression. Peptides 119 23933301
2002 Imaging substance P receptors (NK1) in the living human brain using positron emission tomography. The Journal of clinical psychiatry 114 12562139
1998 Cloning of BY55, a novel Ig superfamily member expressed on NK cells, CTL, and intestinal intraepithelial lymphocytes. Journal of immunology (Baltimore, Md. : 1950) 114 9743336
2006 Molecular and genetic basis for strain-dependent NK1.1 alloreactivity of mouse NK cells. Journal of immunology (Baltimore, Md. : 1950) 110 16751398
2002 Engagement of CD160 receptor by HLA-C is a triggering mechanism used by circulating natural killer (NK) cells to mediate cytotoxicity. Proceedings of the National Academy of Sciences of the United States of America 109 12486241
2015 CD160 is essential for NK-mediated IFN-γ production. The Journal of experimental medicine 95 25711213
2003 Substance P via NK1 receptor facilitates hyperactive bladder afferent signaling via action of ROS. American journal of physiology. Renal physiology 88 12620925
2006 Long-term retention of mature NK1.1+ NKT cells in the thymus. Journal of immunology (Baltimore, Md. : 1950) 87 16547241
1997 NK1.1+ CD4+ T cells lose NK1.1 expression upon in vitro activation. Journal of immunology (Baltimore, Md. : 1950) 77 9164926
2013 CD160 activation by herpesvirus entry mediator augments inflammatory cytokine production and cytolytic function by NK cells. Journal of immunology (Baltimore, Md. : 1950) 75 23761635
2011 The NK-1 receptor: a new target in cancer therapy. Current drug targets 73 21226668
2002 The NK1 receptor mediates both the hyperalgesia and the resistance to morphine in mice lacking noradrenaline. Proceedings of the National Academy of Sciences of the United States of America 71 11805341
2014 CD160-associated CD8 T-cell functional impairment is independent of PD-1 expression. PLoS pathogens 68 25255144
2011 CD160: a unique activating NK cell receptor. Immunology letters 66 21324341
2005 Do substance P and the NK1 receptor have a role in depression and anxiety? Current pharmaceutical design 66 15892660
2001 Localization of NK1 and NK3 receptors in guinea-pig brain. Regulatory peptides 60 11179779
2003 Aprepitant--a novel NK1-receptor antagonist. Expert opinion on pharmacotherapy 56 14640927
2002 BY55/CD160 acts as a co-receptor in TCR signal transduction of a human circulating cytotoxic effector T lymphocyte subset lacking CD28 expression. International immunology 55 11978774
2001 The NK1 receptor is essential for the full expression of noxious inhibitory controls in the mouse. The Journal of neuroscience : the official journal of the Society for Neuroscience 53 11157089
2000 The role of tachykinins via NK1 receptors in progression of human gliomas. Life sciences 51 10954033
2002 Clinical experience with substance P receptor (NK1) antagonists in depression. The Journal of clinical psychiatry 50 12562140
2009 Identification and characterization of a transmembrane isoform of CD160 (CD160-TM), a unique activating receptor selectively expressed upon human NK cell activation. Journal of immunology (Baltimore, Md. : 1950) 49 19109136
2005 Visualization and quantification of neurokinin-1 (NK1) receptors in the human brain. Molecular imaging and biology 48 16155744
2002 Behavioral and physiologic effects of genetic or pharmacologic inactivation of the substance P receptor (NK1). The Journal of clinical psychiatry 48 12562138
1994 BY55 monoclonal antibody delineates within human cord blood and bone marrow lymphocytes distinct cell subsets mediating cytotoxic activity. Proceedings of the National Academy of Sciences of the United States of America 48 8090781
2018 Reduced CD160 Expression Contributes to Impaired NK-cell Function and Poor Clinical Outcomes in Patients with HCC. Cancer research 47 30232222
1996 Expression of tachykinin NK1 receptor mRNA in dorsal root ganglia of the mouse. Brain research. Molecular brain research 47 8717372
2002 The murine neurokinin NK1 receptor gene contributes to the adult hypoxic facilitation of ventilation. The European journal of neuroscience 46 12492418
2014 NK1 receptor antagonists as a new treatment for corneal neovascularization. Investigative ophthalmology & visual science 44 25228541
2002 New insights into the antidepressant actions of substance P (NK1 receptor) antagonists. Canadian journal of physiology and pharmacology 44 12056558
2021 Expanded antigen-experienced CD160+CD8+effector T cells exhibit impaired effector functions in chronic lymphocytic leukemia. Journal for immunotherapy of cancer 42 33931471
2010 CD160 signaling mediates PI3K-dependent survival and growth signals in chronic lymphocytic leukemia. Blood 42 20164468
2002 Elucidating the antidepressant actions of substance P (NK1 receptor) antagonists. Current opinion in investigational drugs (London, England : 2000) 42 12020057
2015 NK-1 Antagonists and Itch. Handbook of experimental pharmacology 41 25861784
2006 The co-expression of 2B4 (CD244) and CD160 delineates a subpopulation of human CD8+ T cells with a potent CD160-mediated cytolytic effector function. European journal of immunology 41 16917959
2014 Involvement of substance P and the NK-1 receptor in pancreatic cancer. World journal of gastroenterology 40 24605029
2006 Characterization of murine CD160+ CD8+ T lymphocytes. Immunology letters 40 16764942
2012 The NK1 receptor antagonist L822429 reduces heroin reinforcement. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 39 23303056
2011 Differential and tumor-specific expression of CD160 in B-cell malignancies. Blood 38 21715317
2007 Peripheral tachykinins and the neurokinin receptor NK1 are required for platelet thrombus formation. Blood 37 17895403
2021 Granzyme A and CD160 expression delineates ILC1 with graded functions in the mouse liver. European journal of immunology 36 34347289
2014 Netupitant and palonosetron trigger NK1 receptor internalization in NG108-15 cells. Experimental brain research 36 24969614
2011 A novel antiangiogenic and vascular normalization therapy targeted against human CD160 receptor. The Journal of experimental medicine 36 21482699
2019 Structural Basis of CD160:HVEM Recognition. Structure (London, England : 1993) 35 31230945
2008 17beta-estradiol suppresses cytotoxicity and proliferative capacity of murine splenic NK1.1+ cells. Cellular & molecular immunology 34 18954559
1994 NK1 receptor expression by cholinergic interneurones in human striatum. Neuroreport 34 7819527
2019 NK-1 Receptor Antagonists and Pruritus: Review of Current Literature. Dermatology and therapy 33 31190215
2019 CD160 serves as a negative regulator of NKT cells in acute hepatic injury. Nature communications 32 31332204
2018 Crystal structure of the human NK1 tachykinin receptor. Proceedings of the National Academy of Sciences of the United States of America 32 30538204
2017 NK1 receptor antagonists for depression: Why a validated concept was abandoned. Journal of affective disorders 32 28753469
2015 Elevated Expression of CD160 and 2B4 Defines a Cytolytic HIV-Specific CD8+ T-Cell Population in Elite Controllers. The Journal of infectious diseases 32 25883386
2019 The Significance of NK1 Receptor Ligands and Their Application in Targeted Radionuclide Tumour Therapy. Pharmaceutics 31 31480582
2009 Murine endometrial and decidual NK1.1+ natural killer cells display a B220+CD11c+ cell surface phenotype. Biology of reproduction 31 19369645
1994 Characterization of NK1 and NK2 tachykinin receptors in guinea-pig and rat bronchopulmonary and vascular systems. British journal of pharmacology 31 7517328
2018 CD160 Stimulates CD8+ T Cell Responses and Is Required for Optimal Protective Immunity to Listeria monocytogenes. ImmunoHorizons 30 31022694
2007 CD160-activating NK cell effector functions depend on the phosphatidylinositol 3-kinase recruitment. International immunology 30 17307798
2000 Tachykinin NK1 and NK3 receptors in the prefrontal cortex of the human brain. Clinical and experimental pharmacology & physiology 29 11071316
2023 TCRαβ+NK1.1-CD4-CD8- double-negative T cells inhibit central and peripheral inflammation and ameliorate ischemic stroke in mice. Theranostics 28 36793857
2007 Identification of a novel CD160+ CD4+ T-lymphocyte subset in the skin: a possible role for CD160 in skin inflammation. The Journal of investigative dermatology 28 17218942
2006 [3H]GR205171 displays similar NK1 receptor binding profile in gerbil and human brain. British journal of pharmacology 28 16501582
2003 VR1-positive primary afferents contact NK1-positive spinoparabrachial neurons. The Journal of comparative neurology 28 12687689
2002 The human tachykinin NK1 (short form) and tachykinin NK4 receptor: a reappraisal. European journal of pharmacology 28 11864635
2002 Neurokinin NK1- and NK3-immunoreactive neurons in serotonergic cell groups in the rat brain. Neuroscience letters 28 11950514
2018 Herpes Simplex Virus 1 Latency and the Kinetics of Reactivation Are Regulated by a Complex Network of Interactions between the Herpesvirus Entry Mediator, Its Ligands (gD, BTLA, LIGHT, and CD160), and the Latency-Associated Transcript. Journal of virology 27 30282707
1997 Generation of NK1.1+ T cell antigen receptor alpha/beta+ thymocytes associated with intact thymic structure. Proceedings of the National Academy of Sciences of the United States of America 27 9122219
2019 Carboplatin chemoresistance is associated with CD11b+/Ly6C+ myeloid release and upregulation of TIGIT and LAG3/CD160 exhausted T cells. Molecular immunology 26 31862674
2006 NK1 receptor antagonists under investigation for the treatment of affective disorders. Expert opinion on investigational drugs 26 16634686
2021 HVEM structures and mutants reveal distinct functions of binding to LIGHT and BTLA/CD160. The Journal of experimental medicine 25 34709351
2014 CD160 isoforms and regulation of CD4 and CD8 T-cell responses. Journal of translational medicine 25 25179432
2009 NK1 receptor antagonism and emotional processing in healthy volunteers. Journal of psychopharmacology (Oxford, England) 25 19351798
2001 Differential expression of functionally identified and immunohistochemically identified NK(1) receptors on sympathetic neurons. Journal of neurophysiology 24 11353005
1993 Identification of both NK1 and NK2 receptors in guinea-pig airways. British journal of pharmacology 24 7694756
2020 CD160 expression on CD8+ T cells is associated with active effector responses but limited activation potential in pancreatic cancer. Cancer immunology, immunotherapy : CII 23 32055919
2018 iNKT Cells Suppress Pathogenic NK1.1+CD8+ T Cells in DSS-Induced Colitis. Frontiers in immunology 23 30333822
1998 Natural killer cell proliferation induced by anti-NK1.1 and IL-2. Immunology and cell biology 23 9619484
1996 Functional characterization of NK1.1 + Ly-6C+ cells. Immunology letters 23 9030975
2020 lncRNA-CD160 decreases the immunity of CD8+ T cells through epigenetic mechanisms in hepatitis B virus infection. Oncology letters 22 32565950
2005 Differentiation of NK1 and NK2 cells. Critical reviews in immunology 22 16167886
2001 NK1 receptor and the ventral medulla of the rat: bulbospinal and catecholaminergic neurons. Neuroreport 22 11726770

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