Affinage

KIR3DS1

Killer cell immunoglobulin-like receptor 3DS1 · UniProt Q14943

Length
382 aa
Mass
42.5 kDa
Annotated
2026-06-10
42 papers in source corpus 18 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/8 claims corpus-supported (88%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIR3DS1 is an activating killer-cell immunoglobulin-like receptor that arms NK cells to recognize and eliminate virus-infected cells through the open-conformer ligand HLA-F (PMID:27455421, PMID:34533978). Lacking an intrinsic signaling domain, KIR3DS1 associates with the ITAM-bearing adaptor DAP12, which is required for both its surface expression and its capacity to trigger cytotoxicity and IFN-γ production (PMID:17202323, PMID:17301953). Antibody-mediated ligation of KIR3DS1 on primary NK cells drives degranulation (CD107a) and cytokine output, confirming its bona fide activating function (PMID:17641029). Biochemical screening of the HLA class I repertoire identified peptide-free, β2-microglobulin-free HLA-F open conformers as the physiological ligand, a specificity confirmed by surface plasmon resonance and pulldown that distinguishes KIR3DS1 from the inhibitory paralog KIR3DL1 (PMID:27455421, PMID:27649529). Because HLA-F is strongly upregulated on cells infected with HIV-1, HCV, BK polyomavirus, and adenovirus, the KIR3DS1/HLA-F axis enables NK cell-mediated control of these infections across cell-culture, humanized-mouse, organoid, and primary-tissue systems (PMID:30031767, PMID:31270222, PMID:33359499, PMID:34533978). HIV-1 subverts this recognition by loading HLA-F with hemoglobin-derived peptides, which abolishes KIR3DS1 binding, whereas removing peptide to regenerate open conformers restores it — a molecular basis for viral immune evasion (PMID:33126487). KIR3DS1 binding to canonical peptide-loaded HLA-Bw4 is weak and allele/peptide-restricted, with most allotypes failing to bind classical HLA-Bw4 tetramers and only rare variants or specific HIV-derived peptide complexes supporting interaction (PMID:17202323, PMID:21804024, PMID:25740999). Consistent with these molecular findings, KIR3DS1 in combination with HLA-B Bw4-80Ile alleles is genetically associated with delayed progression to AIDS in HIV-1 infection (PMID:12134147).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2002 Medium

    Established the first functional clue that KIR3DS1 shapes antiviral immunity, showing a genetic interaction with HLA-B Bw4-80Ile that predicts the rate of HIV disease progression and motivating the search for a ligand and mechanism.

    Evidence Genetic epistasis analysis with KIR/HLA genotyping and Cox regression in a large HIV-1 cohort

    PMID:12134147

    Open questions at the time
    • Statistical association only; no direct receptor-ligand interaction demonstrated
    • Did not identify the molecular ligand or signaling pathway
  2. 2007 High

    Defined KIR3DS1 as an activating receptor by showing it associates with DAP12, depends on DAP12 for surface expression, and triggers cytotoxicity, IFN-γ and degranulation upon ligation.

    Evidence Cotransfection/coimmunoprecipitation in NKL cells, DAP12-dependent transfection, and antibody cross-linking functional assays on primary NK cells

    PMID:17202323 PMID:17301953 PMID:17641029

    Open questions at the time
    • Physiological ligand not identified
    • Antibody ligation does not establish the natural activating stimulus
  3. 2007 Medium

    Ruled out classical peptide-loaded HLA-Bw4 as a straightforward ligand, showing soluble KIR3DS1 and KIR3DS1-expressing cells fail to bind HLA-Bw4 transfectants or HIV-specific HLA-Bw4 tetramers, redirecting the field toward a non-canonical ligand.

    Evidence Soluble KIR3DS1-Ig binding and MHC-I tetramer binding assays on transfected cell lines

    PMID:17202323 PMID:17411378

    Open questions at the time
    • Negative results do not exclude peptide-restricted or low-affinity interactions
    • True ligand remained unknown
  4. 2009 Medium

    Distinguished KIR3DS1 from inhibitory KIR3DL1 functionally, showing KIR3DS1+ NK proliferation and cytotoxicity are inducible by cytokines and stimulator cells but independent of target-cell HLA-Bw4.

    Evidence NK cell proliferation/cytotoxicity assays under cytokine and cell-line stimulation

    PMID:19454667

    Open questions at the time
    • Did not identify an activating ligand
    • HLA-Bw4 independence left the relevant ligand undefined
  5. 2011 High

    Provided the first direct KIR3DS1-HLA-Bw4 binding evidence using a rare allotype and mapped key specificity-determining residues, showing binding is allele-dependent and governed by particular extracellular positions.

    Evidence Flow cytometry binding with KIR3DS1*014 plus site-directed mutagenesis of positions 138 and 199

    PMID:21804024

    Open questions at the time
    • Binding restricted to a rare allotype, not generalizable
    • Functional consequence of this binding not established
  6. 2015 Medium

    Refined the HLA-Bw4 relationship by showing KIR3DS1 can engage HLA-B*57:01 in a strictly peptide-dependent manner via specific HIV-derived epitopes, and that D0-domain polymorphisms reduce HLA-Bw4 binding and surface expression.

    Evidence Structure-driven peptide tetramer binding assays and mutagenesis of D0 residues 58/92 in KIR3DL1/KIR3DS1 chimeras

    PMID:25740999 PMID:26109640

    Open questions at the time
    • Peptide-dependent HLA-Bw4 binding is weak and context-restricted
    • Did not yet identify the dominant physiological ligand
  7. 2016 High

    Identified HLA-F open conformers as the primary physiological ligand, resolving the long-standing ligand question and explaining KIR3DS1's failure to bind classical peptide-loaded MHC-I.

    Evidence Screen of 100 HLA proteins, surface plasmon resonance, biochemical pulldown, and primary NK functional/HIV-inhibition assays; independently replicated by SPR and pulldown

    PMID:27455421 PMID:27649529

    Open questions at the time
    • Structural basis of the KIR3DS1/HLA-F open-conformer interface not resolved
    • Regulation of HLA-F open-conformer generation in vivo not fully defined
  8. 2017 Medium

    Showed that KIR3DS1 can deliver activating signals upon recognizing HLA-B*51 (Bw4-I80) on target cells, but only in HLA-Bw4-I80-negative individuals, highlighting context-dependent activation.

    Evidence NK clone killing/cytokine assays with antibody blockade of KIR3DS1 and NKG2D

    PMID:28603523

    Open questions at the time
    • Relationship between HLA-Bw4 activation and HLA-F-dependent activation not reconciled
    • Partial inhibition by blocking leaves additional receptors contributing
  9. 2018 High

    Demonstrated the KIR3DS1/HLA-F axis is sufficient to activate NK cells against virus-infected targets, with HLA-F upregulation on HCV-infected cells driving NK control and direct ligation sufficient for activation.

    Evidence HCV cell culture, humanized mouse liver and primary tissue models; HLA-F-null 721.221 activation with KIR3DS1-Fc and anti-HLA-F blockade on primary NK cells

    PMID:29743316 PMID:30031767

    Open questions at the time
    • Quantitative contribution relative to other NK receptors in vivo not isolated
    • Signaling steps downstream of DAP12 not dissected
  10. 2019 High

    Confirmed the axis operates in an autologous, biologically relevant setting, showing HLA-F on HIV-infected CD4+ T cells activates KIR3DS1+ NK cells and that blocking the interaction abolishes activation.

    Evidence Coculture of sorted autologous HIV-infected CD4+ T cells with primary NK cells, two independent blocking reagents, exclusive gating

    PMID:31270222

    Open questions at the time
    • In vivo impact on viral reservoir not measured
    • Does not address evasion mechanisms
  11. 2020 Medium

    Extended the axis to additional pathogens and revealed a viral evasion mechanism: BK polyomavirus upregulates HLA-F to enhance KIR3DS1 activation, while HIV exploits hemoglobin-derived peptide loading of HLA-F to abrogate KIR3DS1 binding.

    Evidence BK polyomavirus infection model with patient kidney biopsies; recombinant KIR3DS1 binding with acid peptide elution and mass spectrometry on HLA-F-expressing K562 cells

    PMID:33126487 PMID:33359499

    Open questions at the time
    • Peptide-loading evasion shown with recombinant binding, limited replication
    • Whether peptide loading is virally directed versus a cellular stress response not established
  12. 2021 High

    Generalized the KIR3DS1/HLA-F axis as a broad antiviral surveillance mechanism, showing adenovirus-induced HLA-F upregulation enables KIR3DS1+ NK killing of infected epithelium.

    Evidence 3D intestinal organoid HAdV5 infection model with NK killing assays

    PMID:34533978

    Open questions at the time
    • Pathogen-specific signals driving HLA-F induction not defined
    • In vivo relevance for adenoviral disease not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DAP12-coupled signaling is quantitatively triggered by HLA-F open conformers, the structural basis of the interaction, and how peptide loading of HLA-F is regulated during infection remain to be defined.
  • No structural model of the KIR3DS1/HLA-F complex
  • Downstream DAP12 signaling cascade not dissected
  • Cellular control of HLA-F open-conformer abundance not resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0001618 virus receptor activity 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-168256 Immune System 4
Partners
DAP12HLA-BHLA-F

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 KIR3DS1 associates with the ITAM-bearing adaptor protein DAP12, demonstrated by cotransfection and coimmunoprecipitation experiments in NKL cells. KIR3DS1 expressed on NK cells triggers both cytotoxicity and IFN-gamma production. Cotransfection and coimmunoprecipitation; flow cytometry; in vitro cytotoxicity and cytokine production assays Journal of immunology (Baltimore, Md. : 1950) High 17202323
2007 Surface expression of KIR3DS1 on NK cells is dependent on the adaptor protein DAP12, shown by transfection experiments. KIR3DS1 is recognized by the antibody Z27 on freshly isolated circulating NK cells from KIR3DS1/KIR3DS1 homozygous donors. Transfection; flow cytometry with antibody Z27 and DX9 European journal of immunology Medium 17301953
2007 Ligation of KIR3DS1 by the Z27 antibody on primary NK cells leads to IFN-gamma production and degranulation (CD107a expression), confirming its activating function. KIR3DS1 is also expressed on a small subset of CD56+ T cells. Flow cytometry; NK cell activation assays (IFN-gamma, CD107a); antibody cross-linking Journal of immunology (Baltimore, Md. : 1950) Medium 17641029
2007 KIR3DS1 (as soluble Ig fusion protein) did not bind to EBV-transformed B lymphoid cell lines transfected with HLA-Bw4 80I or 80T allotypes, indicating that if KIR3DS1 recognizes HLA-Bw4 ligands, this interaction is peptide dependent. Soluble KIR3DS1-Ig fusion protein binding assay; flow cytometry on HLA-Bw4-transfected cell lines Journal of immunology (Baltimore, Md. : 1950) Medium 17202323
2007 KIR3DS1 did not bind to a diverse panel of HIV-1-specific HLA-Bw4Ile80 MHC class I tetramers (including various HLA allotypes and peptide epitopes) in 293-T cells transiently expressing KIR3DS1, suggesting KIR3DS1 does not recognize standard peptide-loaded HLA-Bw4 complexes. Flow cytometry; MHC class I tetramer binding assay on KIR3DS1-transfected 293-T cells AIDS research and human retroviruses Medium 17411378
2009 KIR3DS1 expression on NK cells can be induced (upregulated) after exposure to stimulator cells (721.221, K562, EBV-B cell lines, B cells), polyinosinic-polycytidylic acid, IL-15, or IL-2. KIR3DS1+ NK cell proliferation and cytotoxicity were not influenced by the presence of HLA-Bw4 on target cells, in contrast to KIR3DL1+ NK cells. Flow cytometry; NK cell proliferation and cytotoxicity assays; stimulation with cytokines and cell lines Journal of immunology (Baltimore, Md. : 1950) Medium 19454667
2011 The rare KIR3DS1 allotype KIR3DS1*014 directly binds HLA-Bw4, providing the first evidence of direct KIR3DS1-HLA-Bw4 binding. Mutagenesis revealed that position 138 is a key determinant of ligand specificity for KIR3DS1, and that reactivity is dictated by complex interactions between residues at positions 138 and 199. Flow cytometry binding assay; site-directed mutagenesis; recombinant protein analysis Journal of immunology (Baltimore, Md. : 1950) High 21804024
2015 KIR3DS1 recognizes HLA-B*57:01 in a peptide-dependent manner. Using a structure-driven approach, specific HIV-derived peptide epitopes were identified that facilitate productive KIR3DS1-HLA-B*57:01 interactions, establishing that KIR3DS1 ligands exist within the HIV-specific peptide repertoire. Structure-driven peptide analysis; flow cytometry binding assays with HLA-B*57:01 tetramers and KIR3DS1-expressing cells Journal of virology Medium 25740999
2015 KIR3DS1-specific polymorphisms at positions 58 and 92 in the D0 extracellular domain, when introduced into KIR3DL1*009, cause reduced surface expression and dramatically reduced HLA-Bw4 binding compared to KIR3DL1*001, as shown by mutagenesis. Flow cytometry on primary NK cells and transfected HEK293T cells; recombinant protein binding assays; site-directed mutagenesis Journal of immunology (Baltimore, Md. : 1950) High 26109640
2016 KIR3DS1 binds HLA-F open conformers (peptide-free/beta2-microglobulin-free forms). Biochemical screening of 100 HLA class I proteins identified HLA-F as the ligand; confirmed by surface plasmon resonance and biochemical pulldown. Primary KIR3DS1+ NK cells degranulated and produced antiviral cytokines upon encountering HLA-F and inhibited HIV-1 replication in vitro. HIV-1 infection upregulated HLA-F mRNA but decreased KIR3DS1 binding, suggesting viral immune evasion. HLA-protein screen (100 proteins); surface plasmon resonance; biochemical pulldown; primary NK cell functional assays (degranulation, cytokine production); HIV-1 inhibition assay; flow cytometry Nature immunology High 27455421
2016 KIR3DS1 but not KIR3DL1 physically binds HLA-F and other MHC-I open conformers, measured by surface plasmon resonance and biochemical pulldown from cell lines. KIR3DS1 binding to surface-bound HLA-F increases granule exocytosis in activated NK cells. Surface plasmon resonance; biochemical pulldown; biochemical heterodimerization with recombinant proteins; degranulation assay PloS one High 27649529
2017 KIR3DS1 mediates positive signaling (NK cell activation/killing) upon recognition of HLA-B*51 (Bw4-I80) surface molecules on target cells. This activation occurs only in HLA-Bw4-I80-negative individuals. KIR3DS1-mediated activation was partially inhibited by antibody masking of KIR3DS1, and killing could be further revealed when NKG2D function was reduced by antibody blockade. NK cell clone functional assays (killing, cytokine); antibody blocking of KIR3DS1 and NKG2D; transfected target cell killing assays Frontiers in immunology Medium 28603523
2018 Interactions between KIR3DS1 and its ligand HLA-F activate NK cells to control HCV replication. HLA-F is upregulated on HCV-infected cells, and KIR3DS1/HLA-F interactions contribute to NK cell-mediated control of HCV in cell culture, in humanized mouse livers, and in primary liver tissue from HCV-infected individuals. Cell culture HCV infection model; humanized mouse liver model; primary liver tissue analysis; NK cell functional assays Gastroenterology High 30031767
2018 KIR3DS1+ NK cells from KIR3DS1 homozygotes are activated by HLA-F on HLA-null 721.221 cells to produce CCL4, IFN-γ, and express CD107a. Blocking with KIR3DS1-Fc chimeric protein or anti-HLA-F antibodies reduced this activation, demonstrating HLA-F/KIR3DS1 ligation is sufficient for NK cell activation. NK cell functional assays (CCL4, IFN-γ, CD107a); antibody blocking (KIR3DS1-Fc chimeric protein, anti-HLA-F); flow cytometry with exclusive gating Journal of immunology (Baltimore, Md. : 1950) High 29743316
2019 HLA-F expressed on autologous HIV-infected CD4+ T cells activates primary KIR3DS1+ NK cells (higher frequency than KIR3DS1- NK cells) to produce CCL4, IFN-γ, and express CD107a. Blocking HLA-F on HIV-infected cells with KIR3DS1-Fc chimeric protein or anti-HLA-F antibody reduced KIR3DS1+ NK cell activation, establishing that the HLA-F/KIR3DS1 interaction is sufficient to activate NK cells against HIV-infected cells. Coculture of sorted HIV-infected CD4+ T cells with primary NK cells; antibody/Fc-fusion blocking; flow cytometry with exclusive gating for KIR3DS1+ NK cells Journal of virology High 31270222
2020 BK polyomavirus infection significantly increases surface expression of HLA-F on kidney tubular cells, resulting in increased binding of KIR3DS1 to infected cells and activation of primary KIR3DS1+ NK cells, as shown in cell culture and confirmed in kidney biopsy samples from patients. In vitro BK polyomavirus infection model; flow cytometry (HLA-F expression, KIR3DS1 binding); primary NK cell activation assays; immunohistochemistry of patient kidney biopsies Kidney international Medium 33359499
2020 HLA-F loaded with hemoglobin-derived peptides (which are upregulated in HIV-infected CD4+ T cells) loses affinity for KIR3DS1, while acid elution of peptides (generating open conformers) restores KIR3DS1 binding. This provides a molecular mechanism for HIV immune evasion via peptide-dependent regulation of HLA-F/KIR3DS1 interaction. Recombinant soluble KIR3DS1 binding assays; acid elution of peptides; mass spectrometry proteome analysis; flow cytometry on K562 cells expressing membrane-bound HLA-F alleles International journal of molecular sciences Medium 33126487
2021 HLA-F is strongly upregulated on HAdV5-infected intestinal organoid cells, enabling enhanced killing of infected cells by KIR3DS1+ NK cells. This demonstrates that the KIR3DS1/HLA-F axis mediates NK cell recognition and killing of adenovirus-infected cells. 3D intestinal organoid infection model; flow cytometry (HLA-F upregulation); NK cell killing assays with KIR3DS1+ NK cells Science immunology High 34533978
2002 Genetic epistasis analysis revealed that KIR3DS1 in combination with HLA-B Bw4-80Ile alleles is associated with delayed progression to AIDS in HIV-1-infected individuals, and KIR3DS1 alone (without Bw4-80Ile) was associated with more rapid progression, demonstrating a synergistic epistatic interaction between KIR3DS1 and HLA-B Bw4-80Ile loci. Genetic epistasis analysis in large cohort; KIR and HLA genotyping; Cox proportional hazards regression Nature genetics Medium 12134147

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. Nature genetics 932 12134147
2016 Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1. Nature immunology 191 27455421
2009 HLA class I subtype-dependent expansion of KIR3DS1+ and KIR3DL1+ NK cells during acute human immunodeficiency virus type 1 infection. Journal of virology 157 19386717
2008 Increased proportion of KIR3DS1 homozygotes in HIV-exposed uninfected individuals. AIDS (London, England) 146 18317000
2007 Cutting Edge: KIR3DS1, a gene implicated in resistance to progression to AIDS, encodes a DAP12-associated receptor expressed on NK cells that triggers NK cell activation. Journal of immunology (Baltimore, Md. : 1950) 118 17202323
2016 HLA-F and MHC-I Open Conformers Bind Natural Killer Cell Ig-Like Receptor KIR3DS1. PloS one 98 27649529
2008 Conferral of enhanced natural killer cell function by KIR3DS1 in early human immunodeficiency virus type 1 infection. Journal of virology 93 18305035
2010 Donor activating KIR3DS1 is associated with decreased acute GVHD in unrelated allogeneic hematopoietic stem cell transplantation. Blood 83 20124216
2015 Peptide-Dependent Recognition of HLA-B*57:01 by KIR3DS1. Journal of virology 70 25740999
2005 The silent KIR3DP1 gene (CD158c) is transcribed and might encode a secreted receptor in a minority of humans, in whom the KIR3DP1, KIR2DL4 and KIR3DL1/KIR3DS1 genes are duplicated. European journal of immunology 66 15580659
2013 KIR3DS1/L1 and HLA-Bw4-80I are associated with HIV disease progression among HIV typical progressors and long-term nonprogressors. BMC infectious diseases 63 24059286
2009 Role of natural killer cells in a cohort of elite suppressors: low frequency of the protective KIR3DS1 allele and limited inhibition of human immunodeficiency virus type 1 replication in vitro. Journal of virology 62 19211742
2007 Lack of KIR3DS1 binding to MHC class I Bw4 tetramers in complex with CD8+ T cell epitopes. AIDS research and human retroviruses 60 17411378
2007 Allelic expression patterns of KIR3DS1 and 3DL1 using the Z27 and DX9 antibodies. European journal of immunology 54 17301953
2010 Association of the KIR3DS1*013 and KIR3DL1*004 alleles with susceptibility to ankylosing spondylitis. Arthritis and rheumatism 46 20131260
2007 Detection of KIR3DS1 on the cell surface of peripheral blood NK cells facilitates identification of a novel null allele and assessment of KIR3DS1 expression during HIV-1 infection. Journal of immunology (Baltimore, Md. : 1950) 46 17641029
2018 Interactions Between KIR3DS1 and HLA-F Activate Natural Killer Cells to Control HCV Replication in Cell Culture. Gastroenterology 41 30031767
2012 Role of KIR3DS1 in human diseases. Frontiers in immunology 41 23125843
2009 Phenotypic and functional analyses of KIR3DL1+ and KIR3DS1+ NK cell subsets demonstrate differential regulation by Bw4 molecules and induced KIR3DS1 expression on stimulated NK cells. Journal of immunology (Baltimore, Md. : 1950) 31 19454667
2013 Natural killer KIR3DS1 is closely associated with HCV viral clearance and sustained virological response in HIV/HCV patients. PloS one 30 23613999
2011 Analysis of binding of KIR3DS1*014 to HLA suggests distinct evolutionary history of KIR3DS1. Journal of immunology (Baltimore, Md. : 1950) 25 21804024
2017 KIR3DS1-Mediated Recognition of HLA-*B51: Modulation of KIR3DS1 Responsiveness by Self HLA-B Allotypes and Effect on NK Cell Licensing. Frontiers in immunology 24 28603523
2014 Time to seroconversion in HIV-exposed subjects carrying protective versus non protective KIR3DS1/L1 and HLA-B genotypes. PloS one 21 25330014
2019 HLA-F on Autologous HIV-Infected Cells Activates Primary NK Cells Expressing the Activating Killer Immunoglobulin-Like Receptor KIR3DS1. Journal of virology 20 31270222
2012 Association of KIR3DS1+HLA-B Bw4Ile80 combination with susceptibility to tuberculosis in Lur population of Iran. Iranian journal of immunology : IJI 18 22426166
2018 HLA-F on HLA-Null 721.221 Cells Activates Primary NK Cells Expressing the Activating Killer Ig-like Receptor KIR3DS1. Journal of immunology (Baltimore, Md. : 1950) 15 29743316
2021 KIR3DS1 directs NK cell-mediated protection against human adenovirus infections. Science immunology 13 34533978
2015 KIR3DS1-Specific D0 Domain Polymorphisms Disrupt KIR3DL1 Surface Expression and HLA Binding. Journal of immunology (Baltimore, Md. : 1950) 13 26109640
2007 A mutation in KIR3DS1 that results in truncation and lack of cell surface expression. Immunogenetics 12 17687550
2020 Upregulation of HLA-F expression by BK polyomavirus infection induces immune recognition by KIR3DS1-positive natural killer cells. Kidney international 11 33359499
2010 The profile of KIR3DL1 and KIR3DS1 alleles in an African American population resembles that found in African populations. Tissue antigens 11 20230527
2008 Investigation of killer cell immunoglobulin-like receptor gene diversity in KIR3DL1 and KIR3DS1 in a transplant population. Tissue antigens 10 18331531
2017 KIR3DS1/HLA-B Bw4-80Ile Genotype Is Correlated with the IFN-α Therapy Response in hepatitis B e antigen-Positive Chronic Hepatitis B. Frontiers in immunology 9 29075265
2014 Protective genotypes in HIV infection reflect superior function of KIR3DS1+ over KIR3DL1+ CD8+ T cells. Immunology and cell biology 8 25112829
2012 In contrast to HIV, KIR3DS1 does not influence outcome in HTLV-1 retroviral infection. Human immunology 8 22609443
2015 Comparison of the KIR3DS1/Bw4 distribution in Chinese healthy and acute myeloid leukemia individuals. Human immunology 6 25636577
2020 The Loss of HLA-F/KIR3DS1 Ligation Is Mediated by Hemoglobin Peptides. International journal of molecular sciences 4 33126487
2026 Activating KIR3DS1: A key Driver of KIR3DL1/HLA-Bw4-Linked risk in CML. Human immunology 0 42034883
2023 Evaluation of KIR3DL1/KIR3DS1 allelic polymorphisms in Kenyan children with endemic Burkitt lymphoma. PloS one 0 37647275
2018 [The favorable effects of KIR3DS1 and Bw4(80Ile) on viral set point and CD4 count decline in HIV-1 patients with acutely infected with HIV-1 infection]. Zhonghua yi xue za zhi 0 30248785
2014 The KIR3DS1*0130105 allele identified using high-resolution sequence-based typing. Tissue antigens 0 24499056
2014 A novel KIR3DS1*0130107 allele isolated by sequencing from an Asian donor. International journal of immunogenetics 0 24775446

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