Affinage

KIR2DS1

Killer cell immunoglobulin-like receptor 2DS1 · UniProt Q14954

Length
304 aa
Mass
33.6 kDa
Annotated
2026-06-10
36 papers in source corpus 14 papers cited in narrative 14 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/6 claims corpus-supported (83%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIR2DS1 is an activating natural killer (NK) cell receptor that recognizes HLA-C group 2 (C2) molecules and triggers NK cell effector functions including IFN-γ production and target cell cytotoxicity (PMID:17617576). Its ligand specificity is narrowly restricted to HLA-C2 complexes, established by systematic screening across 97 HLA-I proteins, and engagement is peptide-dependent—the HLA-C*06:02/SRGPVHHLL complex activates primary KIR2DS1+ NK clones, and KIR2DS1 recognizes HLA-C2 through a mode distinct from its inhibitory counterpart KIR2DL1 (PMID:28424684, PMID:28546555). Upon engaging HLA-C2+ targets, KIR2DS1-derived activating signals dominate over inhibitory input from NKG2A and, in a defined hierarchy, can be overridden by co-expressed inhibitory KIR2DL2/L3, enabling killing of HLA-C2+ dendritic cells and T-cell blasts (PMID:18308713, PMID:21355085). In decidual NK cells, HLA-C2 on trophoblasts activates KIR2DS1+ cells to secrete GM-CSF, which enhances trophoblast migration and provides a mechanism linking the receptor to placentation (PMID:24091323). Tolerance of KIR2DS1+ cells in HLA-C2-homozygous individuals is enforced by co-expression of self-specific inhibitory KIR, restricting anti-HLA-C2 reactivity to clones lacking inhibitory receptors (PMID:23554313). Beyond HLA, a clade of Plasmodium falciparum RIFIN proteins binds the KIR2DS1 extracellular domain to activate NK cells against malaria-infected erythrocytes, demonstrating recognition of a pathogen-derived non-HLA ligand (PMID:40500441).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2007 High

    Established that KIR2DS1 is a genuine activating receptor for HLA-C2 rather than merely reflecting the absence of inhibitory signaling, resolving whether the receptor itself transmits an activating signal.

    Evidence NK clone IFN-γ and cytotoxicity assays with reciprocal anti-HLA-I and anti-KIR2DS1 blocking, plus clones expressing KIR2DS1 but not KIR2DL1 mRNA

    PMID:17617576

    Open questions at the time
    • Did not define the structural or peptide basis of HLA-C2 recognition
    • Signaling adaptor not directly demonstrated in this study
  2. 2010 Medium

    Defined the baseline expression pattern of KIR2DS1 and showed it does not itself educate NK cells in HLA-C2 individuals, distinguishing activating receptor expression from functional competence.

    Evidence Flow cytometry with discriminating antibodies and NK education assays on primary cells stratified by HLA-C genotype

    PMID:20093094

    Open questions at the time
    • Mechanism of tolerance not yet defined at the clone level
    • T cell subset expression role unexplored
  3. 2011 Medium

    Showed that KIR2DS1 activation dominates over NKG2A inhibition and that purified receptor self-associates, beginning to define both the functional signaling hierarchy and a possible oligomerization mechanism.

    Evidence NK clone cytotoxicity with anti-CD158a blocking; circular dichroism, dynamic light scattering, and atomic force microscopy of purified protein

    PMID:18308713 PMID:21912587

    Open questions at the time
    • Oligomerization not validated by functional mutagenesis
    • Dominance shown in single defined clones
  4. 2011 High

    Defined a hierarchical dominance relationship in which KIR2DS1 overrides NKG2A but is suppressed by co-expressed inhibitory KIR2DL2/L3, clarifying how integration of signals dictates killing of physiological targets.

    Evidence NK clone cytotoxicity against HLA-typed DCs and T-cell blasts with defined receptor co-expression

    PMID:21355085

    Open questions at the time
    • Molecular basis of the dominance hierarchy not resolved
    • Did not test all inhibitory receptor combinations
  5. 2013 High

    Identified GM-CSF secretion as the effector output linking KIR2DS1 engagement of trophoblast HLA-C2 to enhanced trophoblast migration, providing a mechanism for the receptor's role in placentation.

    Evidence Microarray of sorted dNK subsets, intracellular FACS and ELISA for GM-CSF, in vitro trophoblast migration assays

    PMID:24091323

    Open questions at the time
    • Signaling pathway from KIR2DS1 to GM-CSF not mapped
    • In vivo placentation effect not directly demonstrated
  6. 2013 Medium

    Demonstrated that KIR2DS1 can transfer CCR7 from allogeneic targets by trogocytosis, revealing a non-classical consequence of receptor engagement that confers migratory capacity.

    Evidence Flow cytometry for CCR7 acquisition and chemotaxis assays with defined allogeneic targets

    PMID:23449637

    Open questions at the time
    • Mechanism of trogocytic transfer not defined
    • In vivo relevance of acquired CCR7 untested
  7. 2013 High

    Established that tolerance of KIR2DS1+ NK cells in HLA-C2-homozygous donors is enforced by co-expression of inhibitory KIR for self-HLA, explaining how autoreactivity is restrained.

    Evidence NK clone cytotoxicity stratified by donor HLA-C genotype with clone-level receptor profiling and post-transplant analysis

    PMID:23554313

    Open questions at the time
    • Molecular basis of clonal tolerance acquisition not defined
    • Does not address tolerance in non-transplant tissue settings
  8. 2016 High

    Showed that KIR2DS1+ dNK cytotoxicity is amplified against HCMV-infected HLA-C2+ stromal cells while infected trophoblasts remain protected, defining context-dependence and immune privilege at the maternal-fetal interface.

    Evidence CD107a degranulation and cytokine assays of sorted dNK subsets against HCMV-infected stromal cells and trophoblasts

    PMID:27956621

    Open questions at the time
    • Basis of trophoblast immune privilege not molecularly resolved
    • Viral factors modulating HLA-C2 not identified here
  9. 2017 High

    Defined the narrow HLA-C2 ligand specificity of KIR2DS1, showed activation requires active viral gene expression in HCMV-infected cells, and distinguished its recognition mode from KIR2DL1.

    Evidence Mouse 2B4 NFAT-GFP reporter expressing KIR2DS1+DAP12, primary NK degranulation, systematic 97-protein HLA screen, and W6/32 blocking

    PMID:28424684

    Open questions at the time
    • Viral gene product driving activation not identified
    • Structural basis of differential recognition vs KIR2DL1 not resolved
  10. 2017 High

    Demonstrated peptide-dependent engagement of KIR2DS1 by identifying a specific peptide (SRGPVHHLL) presented by HLA-C*06:02 that activates primary KIR2DS1+ clones, establishing that the receptor reads the HLA-bound peptide.

    Evidence KIR2DS1ζ Jurkat reporter with peptide-pulsed TAP1-KO HLA-C*06:02 cells and primary NK clone activation

    PMID:28546555

    Open questions at the time
    • Endogenous peptide repertoire engaging KIR2DS1 not catalogued
    • Structural mode of peptide discrimination not resolved
  11. 2019 Medium

    Using allotype-discriminating antibodies, separated KIR2DS1 from KIR2DL1 at the cell surface and showed differential ligand-induced downregulation, refining how activating and inhibitory counterparts respond to HLA-C2.

    Evidence Flow cytometry with novel discriminating monoclonal antibodies across 230 donors and NK functional assays

    PMID:31024561

    Open questions at the time
    • Mechanism of differential receptor downregulation not defined
    • Functional consequence of retained KIR2DS1 surface levels unclear
  12. 2024 Medium

    Revealed that KIR2DS1 expression intrinsically represses CD16-triggered ADCC independently of NK education, indicating an unexpected dampening role for this activating receptor in antibody-mediated killing.

    Evidence CD107a degranulation assays with rituximab and a CD34xCD16 bispecific engager across defined NK subsets and tumor lines

    PMID:38240527

    Open questions at the time
    • Molecular mechanism of ADCC repression not identified
    • Single lab, requires independent confirmation
  13. 2025 High

    Extended KIR2DS1 ligand recognition beyond HLA by showing a clade of P. falciparum RIFIN proteins binds the receptor and activates NK cells against malaria-infected erythrocytes.

    Evidence RIFIN-KIR2DS1 binding studies, structural analysis of binding surfaces, and NK activation assays with RIFIN-displaying infected erythrocytes

    PMID:40500441

    Open questions at the time
    • In vivo relevance to malaria control not established
    • Affinity and signaling kinetics versus HLA-C2 engagement not compared

Open questions

Synthesis pass · forward-looking unresolved questions
  • The proximal signaling pathway from KIR2DS1/DAP12 engagement to downstream effector outputs (cytotoxicity, GM-CSF, ADCC repression) and the structural basis of peptide-dependent HLA-C2 discrimination remain to be mechanistically resolved.
  • No structural model of KIR2DS1-HLA-C2-peptide complex in the corpus
  • Signal transduction steps downstream of receptor engagement not mapped
  • Mechanism reconciling activating function with ADCC repression unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 2 GO:0001618 virus receptor activity 1
Localization
GO:0005886 plasma membrane 3
Pathway
R-HSA-168256 Immune System 4
Partners
DAP12HLA-C

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 KIR2DS1-expressing NK cells from donors homozygous for HLA-C1 are activated by target cells expressing the C2 group HLA-C antigens, producing IFN-γ and mediating allocytotoxicity. This activation is blocked by antibodies to both HLA class I and KIR2DS1, confirming direct HLA-C2 recognition by KIR2DS1. NK clones expressing KIR2DS1 mRNA but lacking KIR2DL1 mRNA demonstrate that KIR2DS1 itself (not absence of inhibitory signal) mediates C2-induced IFN-γ production. NK clone functional assays (IFN-γ intracellular staining, cytotoxicity assays), antibody blocking experiments, mRNA expression analysis of KIR2DS1 vs KIR2DL1 in clones Journal of immunology High 17617576
2008 In a characterized alloreactive NK clone, KIR2DS1-mediated activation by HLA-C2 targets overrides NKG2A-mediated inhibitory signaling. Homozygous HLA-C2 targets were lysed more strongly than heterozygous C1/C2 targets. Anti-CD158a (KIR2DS1) antibody blocked lysis, confirming KIR2DS1 as the responsible receptor. NK clone cytotoxicity assays with defined HLA-C2+ targets, anti-KIR2DS1 (CD158a) antibody blocking, receptor expression profiling of the clone International immunology Medium 18308713
2011 KIR2DS1+ NK cells efficiently kill HLA-C2+ myelomonocytic dendritic cells (DCs) and T-cell blasts. In NK clones from C2/C2 Bw4/Bw4 donors, activating signals from KIR2DS1 override inhibitory signals from NKG2A or KIR2DL2/L3 co-expressed on the same clone. In C1/C2 targets, KIR2DS1+ NK cells are inhibited by co-expressed KIR2DL2/L3 but not by NKG2A, defining a hierarchical dominance relationship. NK clone cytotoxicity assays against defined HLA-typed target cells (DCs, T-cell blasts); NK clones with defined receptor co-expression patterns Blood High 21355085
2013 KIR2DS1+ decidual NK (dNK) cells are strongly activated upon binding HLA-C2 on trophoblasts. Activation of KIR2DS1+ dNK cells triggers production of GM-CSF (detected by intracellular FACS and ELISA). GM-CSF in turn enhances migration of primary trophoblast and JEG-3 trophoblast cells in vitro, providing a molecular mechanism for KIR2DS1-mediated improvement of placentation. Microarray analysis revealed distinct gene expression responses in dNK co-expressing KIR2DS1+KIR2DL1 vs. those expressing only KIR2DL1. Microarray transcriptomics of sorted dNK subsets, intracellular FACS for GM-CSF, ELISA for secreted GM-CSF, in vitro trophoblast migration assays (primary trophoblast and JEG-3 cells) The Journal of clinical investigation High 24091323
2013 KIR2DS1+ NK cells acquire CCR7 from allogeneic HLA-C2+ CCR7+ cells (lymphoblastoid cell lines, DCs, T-cell blasts) by trogocytosis, thereby gaining migratory capacity toward lymph node chemokines. This CCR7 uptake is enhanced by KIR2DS1 expression and is diminished by co-expression of inhibitory KIR2DL2/L3 (but not by NKG2A in C2/C2 targets). Flow cytometry for CCR7 surface acquisition by NK cell clones and fresh NK cells co-incubated with defined allogeneic targets; chemotaxis assays toward lymph node chemokines Blood Medium 23449637
2013 NK cells from HLA-C2 homozygous donors expressing KIR2DS1 are frequently tolerant to HLA-C2 (reduced frequency of anti-HLA-C2 reactive clones), whereas donors heterozygous or homozygous for HLA-C1 retain high frequencies of KIR2DS1+ anti-HLA-C2 reactive clones. Anti-HLA-C2 cytotoxicity of KIR2DS1+ clones is nearly exclusively restricted to clones lacking inhibitory KIR, demonstrating that co-expression of inhibitory KIR for self-HLA mediates tolerance of KIR2DS1+ cells. KIR2DS1 single-positive anti-HLA-C2 reactive clones persist post-transplantation in HLA-C2+ recipients. NK clone cytotoxicity assays against HLA-C2+ targets from donors with defined HLA-C genotypes; receptor expression profiling of clones by PCR and flow cytometry; post-transplantation donor NK clone analysis Journal of immunology High 23554313
2016 KIR2DS1+ decidual NK cells acquire higher cytotoxic function than KIR2DS1− dNK when exposed to HCMV-infected decidual stromal cells, particularly when stromal cells express HLA-C2. Primary fetal extravillous trophoblasts infected with HCMV did not trigger dNK degranulation or cytokine secretion regardless of KIR2DS1 status, indicating immune privilege limits trophoblast killing even upon viral infection. Degranulation assays (CD107a), cytokine secretion assays of sorted KIR2DS1+ vs KIR2DS1− dNK co-cultured with HCMV-infected decidual stromal cells and primary fetal extravillous trophoblasts; HLA-C2 expression on target cells verified Proceedings of the National Academy of Sciences of the United States of America High 27956621
2017 KIR2DS1 reporter cells (mouse 2B4 carrying NFAT-GFP with KIR2DS1 and modified DAP12) and primary KIR2DS1+ NK cells are activated specifically by C2-HLA-C+ fibroblasts infected with specific clones of a clinical HCMV strain, but not by uninfected fibroblasts or HLA-C-transfected 721.221 cells. Active viral gene expression is required for KIR2DS1 activation. Anti-HLA class I (W6/32) blocks KIR2DS1 reporter activation but does not block KIR2DL1, indicating differential HLA-C recognition modes by KIR2DS1 vs KIR2DL1. KIR2DS1 binding was restricted to HLA-C group 2 complexes in a systematic screen of 97 HLA-I proteins. Mouse 2B4 NFAT-GFP reporter cell system expressing KIR2DS1+DAP12; primary NK cell degranulation assays; systematic binding screen of 97 HLA-I proteins; antibody blocking with W6/32 Frontiers in immunology High 28424684
2017 KIR2DS1 binding is narrowly restricted to HLA-C group 2 (C2) complexes in a systematic screen of 97 HLA-I proteins, whereas KIR2DL1 shows broader binding specificity. Using KIR2DS1ζ+ Jurkat reporter cells and peptide-pulsed HLA-C*06:02+ TAP1-KO cells, the synthetic peptide SRGPVHHLL presented by HLA-C*06:02 was identified as engaging KIR2DS1. This HLA-C*06:02/SRGPVHHLL complex also activates primary KIR2DS1+ NK cell clones, demonstrating peptide-dependent engagement of KIR2DS1. Systematic HLA binding screen (97 HLA-I proteins); KIR2DS1ζ Jurkat reporter cell assay with peptide-pulsed 721.221.TAP1KO-HLA-C*06:02 cells; primary NK clone activation assays Scientific reports High 28546555
2011 KIR2DS1 self-associates in a well-defined fashion as revealed by circular dichroism spectroscopy, dynamic light scattering, and atomic force microscopy, suggesting receptor oligomerization may contribute to its signaling mechanism. Circular dichroism spectroscopy, dynamic light scattering, atomic force microscopy of purified KIR2DS1 protein PloS one Medium 21912587
2025 A clade of Plasmodium falciparum RIFIN proteins binds to the KIR2DS1 extracellular domain (the RIFIN-binding surface of KIR2DL1 is conserved in KIR2DS1), resulting in activation of KIR2DS1-expressing NK cells. This demonstrates that KIR2DS1 can recognize a pathogen-derived non-HLA ligand and mediates NK cell activation against malaria-infected erythrocytes. Binding studies of RIFIN proteins to KIR2DS1; NK cell activation assays with KIR2DS1-expressing NK cells co-cultured with RIFIN-displaying P. falciparum-infected erythrocytes; structural analysis of RIFIN-KIR binding surfaces Nature High 40500441
2024 KIR2DS1+ NK cells demonstrate dominantly repressed ADCC (CD16-triggered degranulation) toward tumor cell lines in both missing-self and KIR-ligand matched settings, even in the presence of HLA-C2 (its ligand). This repression was also observed when KIR2DS1+ NK cells were stimulated with a CD34xCD16 bispecific killer engager, indicating KIR2DS1 expression intrinsically dampens ADCC independently of educational status. Flow cytometry-based degranulation assays (CD107a) of defined NK cell subsets stimulated with rituximab or CD34xCD16 bispecific killer engager against defined tumor cell lines; NK subset characterization by KIR expression profiling Journal of immunology Medium 38240527
2019 Co-expression of HLA-C2 ligand diminishes KIR2DL1 (but not KIR2DS1) cell surface staining without affecting the frequencies of KIR2DL1- or KIR2DS1-expressing cells within the NK repertoire, revealing differential ligand-induced receptor downregulation between the inhibitory and activating counterparts. Education (tolerization) of KIR2DS1+ NK cells by HLA-C2 can be overridden by co-expression of self-specific inhibitory receptors such as CD94/NKG2A. Flow cytometry with novel allotype-discriminating monoclonal antibodies distinguishing KIR2DL1 and KIR2DS1; analysis of 230 healthy donors; NK functional assays Frontiers in immunology Medium 31024561
2010 KIR2DS1 is expressed on approximately 10% of circulating NK cells in the absence of KIR2DL1, regardless of donor HLA-C genotype. In HLA-C2 individuals, KIR2DS1 does not induce NK cell education (acquisition of competence) and does not interfere with KIR2DL1-induced NK cell education. KIR2DS1 is also present on rare oligoclonal TCRαβ+CD8α+ and TCRαβ+CD4−CD8− T cell subsets. Flow cytometry with discriminating antibodies on primary human NK and T cells from defined HLA-C genotype donors; NK education functional assays Clinical immunology Medium 20093094

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 HLA-C-dependent prevention of leukemia relapse by donor activating KIR2DS1. The New England journal of medicine 360 22931314
2013 Maternal uterine NK cell-activating receptor KIR2DS1 enhances placentation. The Journal of clinical investigation 222 24091323
2007 KIR2DS1-positive NK cells mediate alloresponse against the C2 HLA-KIR ligand group in vitro. Journal of immunology (Baltimore, Md. : 1950) 154 17617576
2004 Gene for the activating natural killer cell receptor, KIR2DS1, is associated with susceptibility to psoriasis vulgaris. Human immunology 126 15310528
2011 Natural killer cells expressing the KIR2DS1-activating receptor efficiently kill T-cell blasts and dendritic cells: implications in haploidentical HSCT. Blood 91 21355085
2016 Expression of KIR2DS1 by decidual natural killer cells increases their ability to control placental HCMV infection. Proceedings of the National Academy of Sciences of the United States of America 73 27956621
2005 Activating killer cell immunoglobulin-like receptor gene KIR2DS1 is associated with psoriatic arthritis. Human immunology 73 16112031
2010 Association of KIR2DS1 and KIR2DS3 with fatal outcome in Ebola virus infection. Immunogenetics 63 20878400
2008 KIR2DS1-mediated activation overrides NKG2A-mediated inhibition in HLA-C C2-negative individuals. International immunology 53 18308713
2013 NK cell tolerance of self-specific activating receptor KIR2DS1 in individuals with cognate HLA-C2 ligand. Journal of immunology (Baltimore, Md. : 1950) 50 23554313
2017 Modulation of Human Leukocyte Antigen-C by Human Cytomegalovirus Stimulates KIR2DS1 Recognition by Natural Killer Cells. Frontiers in immunology 49 28424684
2020 External validation of models for KIR2DS1/KIR3DL1-informed selection of hematopoietic cell donors fails. Blood 43 31932846
2011 KIR2DS1 genotype predicts for complete cytogenetic response and survival in newly diagnosed chronic myeloid leukemia patients treated with imatinib. Leukemia 40 21844874
2013 KIR2DS1-dependent acquisition of CCR7 and migratory properties by human NK cells interacting with allogeneic HLA-C2+ DCs or T-cell blasts. Blood 37 23449637
2017 Peptide-specific engagement of the activating NK cell receptor KIR2DS1. Scientific reports 35 28546555
2019 Novel Approach to Cell Surface Discrimination Between KIR2DL1 Subtypes and KIR2DS1 Identifies Hierarchies in NK Repertoire, Education, and Tolerance. Frontiers in immunology 32 31024561
2013 Protective effect of the KIR2DS1 gene in atopic dermatitis. Gene 32 23831511
2011 KIR3DL1+HLA-B Bw4Ile80 and KIR2DS1+HLA-C2 combinations are both associated with ankylosing spondylitis in the Iranian population. International journal of immunogenetics 26 21797986
2015 Recurrent Pregnancy Loss in Women with Killer Cell Immunoglobulin-Like Receptor KIR2DS1 is Associated with an Increased HLA-C2 Allelic Frequency. American journal of reproductive immunology (New York, N.Y. : 1989) 24 26589762
2010 Expression of the HLA-C2-specific activating killer-cell Ig-like receptor KIR2DS1 on NK and T cells. Clinical immunology (Orlando, Fla.) 23 20093094
2008 A study of the killer cell immunoglobulin-like receptor gene KIR2DS1 in a Caucasoid Brazilian population with psoriasis vulgaris. Tissue antigens 23 18643961
2011 Role of alloreactive KIR2DS1(+) NK cells in haploidentical hematopoietic stem cell transplantation. Journal of leukocyte biology 22 21791599
2006 A role for KIR gene variants other than KIR2DS1 in conferring susceptibility to psoriasis. Human immunology 21 16829306
2018 KIR2DS1, 2DS5, 3DS1 and KIR2DL5 are associated with the risk of head and neck squamous cell carcinoma in Iranians. Human immunology 20 29408295
2014 The role of KIR2DS1 in multiple sclerosis--KIR in Portuguese MS patients. Journal of neuroimmunology 18 24529855
2008 Investigation of killer cell immunoglobulin-like receptor gene diversity, KIR2DL1 and KIR2DS1. Tissue antigens 14 18643963
2016 Multiple sclerosis is accompanied by lack of KIR2DS1 gene: A meta-analysis. Genomics data 13 27747156
2011 Self-association of an activating natural killer cell receptor, KIR2DS1. PloS one 10 21912587
2019 Donor KIR2DS1-Mediated Decreased Relapse and Improved Survival Depending on Remission Status at HLA-Haploidentical Transplantation with Post-Transplantation Cyclophosphamide. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 9 31899360
2022 KIR2DS1-HLA-C status as a predictive marker for benefit from rituximab: a post-hoc analysis of the RICOVER-60 and CLL8 trials. The Lancet. Haematology 7 35114151
2023 Association of KIR2DL5, KIR2DS5, and KIR2DS1 allelic variation and atopic dermatitis. Scientific reports 5 36720995
2019 Donor KIR2DS1 reduces the risk of transplant related mortality in HLA-C2 positive young recipients with hematological malignancies treated by myeloablative conditioning. PloS one 5 31237928
2025 RIFINs displayed on malaria-infected erythrocytes bind KIR2DL1 and KIR2DS1. Nature 4 40500441
2024 KIR2DS1 and KIR2DL1-C245 Dominantly Repress NK Cell Degranulation Triggered by Monoclonal or Bispecific Antibodies, whereas Education by Uptuning Inhibitory Killer Ig-related Receptors Exerts No Advantage in Ab-dependent Cellular Cytotoxicity. Journal of immunology (Baltimore, Md. : 1950) 4 38240527
2017 Expression of KIR2DS1 does not significantly contribute to NK cell cytotoxicity in HLA-C1/C2 heterozygous haplotype B donors. International immunology 4 29099970
2026 Antibody S22019F Selectively Recognises KIR2DS1 and Enables Analysis of KIR2DS1+ NK Cells and T Cells. HLA 0 42125902

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