Affinage

KIR2DL3

Killer cell immunoglobulin-like receptor 2DL3 · UniProt P43628

Length
341 aa
Mass
37.9 kDa
Annotated
2026-06-10
48 papers in source corpus 15 papers cited in narrative 15 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

KIR2DL3 is an inhibitory NK cell receptor whose two tandem Ig-like domains dock onto HLA-C (C1-epitope) allotypes to dampen NK cell effector responses, and whose engagement is exquisitely tuned by both receptor polymorphism and the peptide presented by the HLA-C ligand (PMID:10196125, PMID:33846289). Its extracellular region adopts an acute interdomain elbow angle (~23°) that positions an HLA-C binding site spanning both domains, with the relative domain orientation itself shaping ligand binding (PMID:10196125). Specificity and avidity are partitioned across two classes of residues: positions within the binding site (44, 70, 71, 131) govern HLA specificity, cross-reactivity, and avidity (PMID:22772445), whereas residues distal to the interface (11, 16, 35, 148) modulate the interdomain hinge angle and thereby set overall avidity—such that combining R16P+R148C, or R11+E35, raises KIR2DL3 affinity toward the stronger KIR2DL2-like state and increases inhibition of NK cell IFN-γ production (PMID:18322206, PMID:23686481). Compared with the allotypically related KIR2DL2 and with KIR2DL1, KIR2DL3 has lower avidity, broader HLA-C specificity, and greater mutational adaptability, and the two C1 receptors achieve distinct docking geometries on HLA-C that translate into differential allotype recognition (PMID:22772445, PMID:33846289). Engagement is further controlled by the specific peptide loaded onto HLA-C: peptide identity tunes inhibitory signaling strength, and HLA-presented peptide composition determines whether a given complex forms a KIR2DL3 ligand, including the exceptional HLA-B*46:01 that acquired the C1 epitope by mini-conversion (PMID:28514659, PMID:25359276). This peptide sensitivity provides a route for viral immune escape, as HIV-1 Gag and HCV core peptide variants that enhance KIR2DL3/HLA-C engagement suppress primary KIR2DL3+ NK cell activation (PMID:26575988, PMID:27057987). Beyond NK cells, transgenic and reconstitution-setting studies show KIR2DL3 can also deliver activation-stage-dependent inhibitory signals to T cells (PMID:10498612, PMID:34349169).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1999 High

    Establishing the structural architecture of KIR2DL3 defined how a two-domain receptor presents its HLA-C binding surface, revealing that domain orientation is itself a tunable feature of ligand recognition.

    Evidence X-ray crystallography of the KIR2DL3 extracellular region with comparison to KIR2DL1

    PMID:10196125

    Open questions at the time
    • No co-complex with HLA-C in this study
    • Functional consequence of the acute elbow angle not directly tested
  2. 1999 Medium

    Demonstrating that transgenic KIR2DL3 inhibits T cell cytotoxicity established its inhibitory function beyond NK cells and revealed dependence on the activation stage of the responding T cell.

    Evidence Tg-KIR2DL3 × Tg-HLA-Cw3 mouse model, MLR, and anti-CD3-redirected killing assays

    PMID:10498612

    Open questions at the time
    • Single-lab transgenic system
    • Mechanism of activation-stage dependence unresolved
    • Human T cell relevance not addressed here
  3. 2004 Medium

    Generating a KIR2DL3-specific antibody enabled discrimination of KIR2DL3 from serologically indistinguishable KIR2DL2/S2, allowing receptor-resolved analysis of surface expression and signaling.

    Evidence Monoclonal antibody (ECM41) generation, flow cytometry, and redirected killing in NK cell clones

    PMID:15314042

    Open questions at the time
    • Reagent specificity defined functionally but epitope not yet mapped
    • Single lab
  4. 2008 High

    Mapping the avidity difference between KIR2DL2 and KIR2DL3 to distal residues showed that ligand strength is encoded outside the binding site through interdomain hinge geometry.

    Evidence Site-directed mutagenesis (R16P, R148C) with functional binding across 93 HLA allotypes

    PMID:18322206

    Open questions at the time
    • Hinge-angle change inferred, not structurally resolved here
    • Synergy mechanism between the two positions not visualized
  5. 2010 Medium

    Defining the residues controlling antibody reactivity clarified that unusual mAb staining of KIR2DL3*005 does not reflect altered HLA-C specificity, separating epitope variation from ligand function.

    Evidence Site-directed mutagenesis of positions 35/50 with multi-mAb flow cytometry and functional analysis

    PMID:20525888

    Open questions at the time
    • Functional impact of residue 35 on ligand binding addressed only later
    • Single lab
  6. 2012 High

    Comprehensive mutagenesis of positively selected binding-site residues partitioned specificity, cross-reactivity, and avidity across discrete positions and established KIR2DL3 as more adaptable than KIR2DL1.

    Evidence 38 point mutants assayed for binding against 95 HLA-A/-B/-C allotypes

    PMID:22772445

    Open questions at the time
    • Structural basis of each residue contribution not directly visualized
    • Effect on downstream NK signaling not quantified
  7. 2013 High

    Linking the distal residues 11 and 35 to higher KIR2DL3*005 affinity connected hinge-angle modulation to a measurable increase in NK cell inhibition.

    Evidence Surface plasmon resonance, mutagenesis, and primary NK cell IFN-γ functional assay

    PMID:23686481

    Open questions at the time
    • Hinge-angle change inferred rather than crystallographically confirmed
    • Allele-frequency/clinical consequence not assessed
  8. 2014 Medium

    Showing KIR2DL3+ NK cells are more peptide-sensitive than KIR2DL2+ cells established HLA-bound peptide selectivity as a basis for differential receptor reactivity.

    Evidence Primary NK cell functional assays with defined peptide variants and mathematical modeling

    PMID:25359276

    Open questions at the time
    • Limited peptide panel
    • Structural basis of peptide discrimination not resolved
    • Single lab
  9. 2014 Medium

    Distinguishing KIR2DL3+NKG2A− from NKG2A+ NK cells in HCV infection linked receptor-defined subset identity to differential susceptibility to HLA-E-mediated inhibition and antiviral response.

    Evidence Multicolor flow cytometry, liver HLA-E expression analysis, and primary NK cell IFN-γ assays

    PMID:24780303

    Open questions at the time
    • Correlative subset analysis
    • Direct causal role of KIR2DL3 vs. NKG2A absence not isolated
    • Single lab
  10. 2015 High

    Identifying an HIV-1 Gag escape mutation that strengthens KIR2DL3/HLA-C engagement demonstrated peptide-driven viral immune evasion through enhanced inhibitory receptor signaling.

    Evidence KIR2DL3-Fc binding, primary NK cell activation assay, SPR, and structural modeling in a genotyped cohort

    PMID:26575988

    Open questions at the time
    • In vivo NK-mediated selection pressure inferred from cohort association
    • Structural model not experimentally resolved
  11. 2016 High

    Demonstrating that an HCV core peptide variant alters HLA-C stabilization and KIR2DL3 binding extended peptide-dependent immune escape to a second virus and tied epitope sequence to NK inhibition strength.

    Evidence KIR2DL3-IgG binding, HLA-C*03:04 stabilization assay, and primary NK cell IFN-γ functional assay

    PMID:27057987

    Open questions at the time
    • No structural complex of the variant peptide
    • In vivo selection not directly demonstrated
  12. 2017 Medium

    Showing that HLA-B*46:01 acquired the C1 epitope and serves as a KIR2DL3 ligand for only a peptidome subset established that HLA peptide composition determines ligand formation beyond canonical HLA-C.

    Evidence High-resolution mass spectrometry peptidome analysis with KIR2DL3 binding assays

    PMID:28514659

    Open questions at the time
    • Functional NK consequence of HLA-B*46:01 recognition not quantified
    • Single lab
  13. 2021 High

    Co-crystal structures of KIR2DL2 and KIR2DL3 with HLA-C*07:02 revealed distinct docking geometries, providing the structural basis for differential HLA-C1 allotype recognition by the two C1 receptors.

    Evidence X-ray crystallography of both receptor/HLA-C*07:02 complexes with mutagenesis and primary NK cell functional assays

    PMID:33846289

    Open questions at the time
    • Single HLA-C allotype crystallized
    • Link between docking geometry and signaling magnitude not fully quantified
  14. 2021 Medium

    Demonstrating KIR2DL3 inhibition of CMV-specific T cell responses preferentially against allogeneic C1+ targets extended its inhibitory role to post-transplant T cell immunity.

    Evidence In vitro functional T cell assays comparing allogeneic vs. autologous C1+ targets after haploidentical HSCT

    PMID:34349169

    Open questions at the time
    • Clinical outcome correlation not established
    • Single-lab in vitro setting

Open questions

Synthesis pass · forward-looking unresolved questions
  • How peptide-encoded differences in KIR2DL3 engagement quantitatively translate into NK/T cell activation thresholds in vivo, and whether they shape disease and transplant outcomes, remains unresolved.
  • No structural model of peptide-variant complexes resolved at atomic resolution
  • Causal in vivo selection of escape variants by KIR2DL3+ NK cells not directly demonstrated
  • Clinical consequences of receptor polymorphism not established in the corpus

Mechanism profile

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

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Crystal structure of the extracellular region of KIR2DL3 (p58) was solved, revealing two tandem immunoglobulin-like domains with an unusually acute interdomain elbow angle of 23° different from KIR2DL1. The putative HLA-C binding site spans both domains on the outer surface of the elbow, and the relative domain orientation can modulate the binding site. X-ray crystallography Structure High 10196125
2008 KIR2DL2 binds HLA-C ligands with higher avidity than KIR2DL3 due to synergistic polymorphism at two positions distal to the ligand-binding site: proline 16 in D1 and arginine 148 in D2. Site-directed mutagenesis showed that the combination (but not individual substitutions) of R16P and R148C converts KIR2DL3 into a stronger receptor comparable to KIR2DL2, likely by altering the hinge angle between the two Ig-like domains. Site-directed mutagenesis combined with functional binding assays to 93 HLA allotypes Journal of immunology High 18322206
1999 KIR2DL3 expressed as a transgene in mouse T cells can inhibit mixed lymphocyte reaction and anti-CD3-redirected cytotoxicity by freshly isolated splenocytes upon engagement with its ligand HLA-Cw3. However, antigen- or anti-CD3-induced cytotoxicity by activated alloreactive CTLs could NOT be inhibited by KIR2DL3 engagement, demonstrating that KIR2DL3's inhibitory effect on T cells is activation-stage dependent. Transgenic mouse model (Tg-KIR2DL3 and Tg-KIR2DL3 × Tg-HLA-Cw3 double transgenic), redirected killing assays, MLR, anti-CD3 stimulation Blood Medium 10498612
2004 A novel monoclonal antibody (ECM41) specific for KIR2DL3 was generated and used to show that KIR2DL3 and KIR2DL2 have distinct surface expression patterns and HLA-C specificities that were previously indistinguishable serologically. Simultaneous engagement of KIR2DL3 (inhibitory) and KIR2DS2 (activating) in NK cell clones co-expressing both receptors was functionally assessed using redirected killing assays. Monoclonal antibody generation, flow cytometry, redirected killing assays with NK cell clones International immunology Medium 15314042
2010 Site-directed mutagenesis of KIR2DL3 demonstrated that glutamine at position 35 is required for ECM41 mAb staining, and glutamic acid 35 plus arginine 50 are required for staining by EB6B/11PB6 mAbs. KIR2DL3*005 allele bearing these residues showed HLA-C specificity comparable to other KIR2DL2/L3 alleles despite its unusual antibody reactivity pattern. Site-directed mutagenesis, flow cytometry with multiple mAbs, functional analysis Journal of immunology Medium 20525888
2012 Mutagenesis of six positively selected positions in the HLA class I binding site of KIR2DL3 showed that position 44 modulates specificity for HLA-C, positions 71 and 131 control cross-reactivity with HLA-A*11:02, and position 70 dominates avidity modulation (with lesser contributions from positions 68 and 182). KIR2DL3 has lower avidity and broader specificity than KIR2DL1, and unlike KIR2DL1 its avidity can be increased and specificity changed by mutation, demonstrating its greater adaptability. Site-directed mutagenesis generating 38 point mutants, binding assays to 95 HLA-A, -B, and -C allotypes Journal of immunology High 22772445
2013 KIR2DL3*005 allele binds HLA-C with significantly higher affinity and avidity than KIR2DL3*001, producing stronger inhibition of NK cell IFN-γ production. Site-directed mutagenesis established that the combination of arginine at residue 11 and glutamic acid at residue 35 (both distal to the KIR/HLA-C interface) is critical to this increased affinity, likely by altering the interdomain hinge angle toward that of KIR2DL2. Surface plasmon resonance, flow cytometry, site-directed mutagenesis, NK cell functional assay (IFN-γ) Journal of immunology High 23686481
2015 HIV-1 mutation at p24 Gag position 303 (TGag303V) selected in individuals carrying both KIR2DL3 and HLA-C*03:04 enhanced KIR2DL3 binding to HLA-C*03:04-presenting cells and significantly reduced activation of primary KIR2DL3+ NK cells, demonstrating that peptide sequence variation within HLA-presented epitopes modulates KIR2DL3 inhibitory signaling and mediates viral immune escape. KIR2DL3 binding assay (flow cytometry with KIR2DL3-Fc fusion), primary NK cell activation assay, surface plasmon resonance, structural modeling PLoS medicine High 26575988
2016 An HCV core-derived peptide (YIPLVGAPL) bound to HLA-C*03:04 resulted in significantly higher KIR2DL3 binding and suppression of primary KIR2DL3+ NK cell function. Genotype-specific HCV peptide variants of this sequence showed lower HLA-C*03:04 stabilization, decreased KIR2DL3 binding, and lower NK cell inhibition, demonstrating sequence-dependent modulation of KIR2DL3 engagement by viral peptides. KIR2DL3-IgG fusion construct binding assay, HLA stabilization assay (722.221-HLA-C*03:04 transfectants), primary NK cell IFN-γ functional assay Journal of hepatology High 27057987
2017 HLA-B*46:01 carries the C1 epitope introduced by intergenic mini-conversion from HLA-C*01:02 and is recognized by KIR2DL3. High-resolution mass spectrometry showed that only a minority (21%) of HLA-B*46:01 peptides with specific C-terminal characteristics form ligands for KIR2DL3, demonstrating that peptide composition of the HLA peptidome determines KIR2DL3 ligand formation. High-resolution mass spectrometry peptidome analysis, KIR2DL3 binding assays Cell reports Medium 28514659
2014 KIR2DL3-positive NK cells were more sensitive than KIR2DL2-positive NK cells to changes in the peptide content of MHC class I, with weakly inhibitory peptide VAPWNSRAL discriminating KIR2DL3 from KIR2DL2 donors. Mathematical modeling confirmed VAPWNSRAL dominance in distinguishing the two receptor populations, demonstrating peptide selectivity as a mechanistic basis for differential NK cell reactivity. Primary NK cell functional assays with defined peptide variants, mathematical modeling European journal of immunology Medium 25359276
2021 Crystal structures of KIR2DL2 and KIR2DL3 in complex with HLA-C*07:02 presenting a self-epitope revealed that KIR2DL2 and KIR2DL3 differ in their docking geometry atop HLA-C*07:02. This structural plasticity correlates with differential recognition of HLA-C1 allotypes. Mutagenesis assays confirmed differences in the mechanism of HLA-C1 allotype recognition between KIR2DL2 and KIR2DL3, and primary NK cell inhibition by HLA-C1 allotypes differed markedly. X-ray crystallography of KIR2DL2/HLA-C*07:02 and KIR2DL3/HLA-C*07:02 complexes, mutagenesis assays, primary NK cell functional assays Nature communications High 33846289
2014 KIR2DL3+NKG2A− NK cells were not inhibited by HLA-E ligation (unlike KIR2DL3−NKG2A+ NK cells), and this insensitivity to HLA-E-mediated inhibition was mechanistically linked to their ability to respond to HCV-infected cells. HLA-E upregulation in HCV-infected liver correlated with viral load and suppressed NK cell IFN-γ secretion specifically in NKG2A+ populations. Multicolor flow cytometry (phenotyping and functional assays), liver biopsy HLA-E expression analysis, primary NK cell IFN-γ assays Journal of hepatology Medium 24780303
2021 KIR2DL3 expressed on T lymphocytes during immune reconstitution after haploidentical HSCT showed a higher inhibitory effect on CMV-specific T cell responses against allogeneic than autologous C1+ target cells, demonstrating that KIR2DL3-HLA interactions modulate T cell immune responses in an allogeneic setting. Functional T cell assays, flow cytometry, in vitro KIR2DL3 inhibition of CMV-specific T cell responses against allogeneic vs. autologous C1+ targets Scientific reports Medium 34349169
2022 Differential expression of KIR/NKAT2 (KIR2DL3) between NK cell subsets was documented: CD56dim peripheral blood NK cells express KIR/NKAT2 whereas CD56bright peripheral blood NK cells do not; however, both CD56bright and CD56dim decidual NK cell subsets express KIR/NKAT2 and CD94 in early pregnancy. Flow cytometry on peripheral blood and decidual tissue NK cells from pregnant and non-pregnant women Fertility and sterility Low 15019821

Source papers

Stage 0 corpus · 48 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Synergistic polymorphism at two positions distal to the ligand-binding site makes KIR2DL2 a stronger receptor for HLA-C than KIR2DL3. Journal of immunology (Baltimore, Md. : 1950) 324 18322206
2009 Co-evolution of KIR2DL3 with HLA-C in a human population retaining minimal essential diversity of KIR and HLA class I ligands. Proceedings of the National Academy of Sciences of the United States of America 100 19837691
2012 Diverse functionality among human NK cell receptors for the C1 epitope of HLA-C: KIR2DS2, KIR2DL2, and KIR2DL3. Frontiers in immunology 93 23189078
2013 Large spectrum of HLA-C recognition by killer Ig-like receptor (KIR)2DL2 and KIR2DL3 and restricted C1 SPECIFICITY of KIR2DS2: dominant impact of KIR2DL2/KIR2DS2 on KIR2D NK cell repertoire formation. Journal of immunology (Baltimore, Md. : 1950) 85 24078689
1999 Crystal structure of the human p58 killer cell inhibitory receptor (KIR2DL3) specific for HLA-Cw3-related MHC class I. Structure (London, England : 1993) 81 10196125
2012 Mutation at positively selected positions in the binding site for HLA-C shows that KIR2DL1 is a more refined but less adaptable NK cell receptor than KIR2DL3. Journal of immunology (Baltimore, Md. : 1950) 74 22772445
2015 Selection of an HLA-C*03:04-Restricted HIV-1 p24 Gag Sequence Variant Is Associated with Viral Escape from KIR2DL3+ Natural Killer Cells: Data from an Observational Cohort in South Africa. PLoS medicine 71 26575988
2013 Allelic variation in KIR2DL3 generates a KIR2DL2-like receptor with increased binding to its HLA-C ligand. Journal of immunology (Baltimore, Md. : 1950) 61 23686481
2007 Natural killer cells in perinatally HIV-1-infected children exhibit less degranulation compared to HIV-1-exposed uninfected children and their expression of KIR2DL3, NKG2C, and NKp46 correlates with disease severity. Journal of immunology (Baltimore, Md. : 1950) 58 17709553
2012 Significant association of KIR2DL3-HLA-C1 combination with cerebral malaria and implications for co-evolution of KIR and HLA. PLoS pathogens 52 22412373
2021 Structural plasticity of KIR2DL2 and KIR2DL3 enables altered docking geometries atop HLA-C. Nature communications 48 33846289
2016 Sequence variations in HCV core-derived epitopes alter binding of KIR2DL3 to HLA-C∗03:04 and modulate NK cell function. Journal of hepatology 40 27057987
2017 The Intergenic Recombinant HLA-B∗46:01 Has a Distinctive Peptidome that Includes KIR2DL3 Ligands. Cell reports 39 28514659
2014 KIR2DL3⁺NKG2A⁻ natural killer cells are associated with protection from productive hepatitis C virus infection in people who inject drugs. Journal of hepatology 32 24780303
2010 Combined genotypic and phenotypic killer cell Ig-like receptor analyses reveal KIR2DL3 alleles displaying unexpected monoclonal antibody reactivity: identification of the amino acid residues critical for staining. Journal of immunology (Baltimore, Md. : 1950) 30 20525888
1999 Modulation of T-cell functions in KIR2DL3 (CD158b) transgenic mice. Blood 30 10498612
2014 Peptide selectivity discriminates NK cells from KIR2DL2- and KIR2DL3-positive individuals. European journal of immunology 29 25359276
2015 KIR2DL3 and KIR2DL1 show similar impact on licensing of human NK cells. European journal of immunology 25 26467237
2017 KIR2DL3 and the KIR ligand groups HLA-A-Bw4 and HLA-C2 predict the outcome of hepatitis B virus infection. Journal of viral hepatitis 24 28211154
2019 Killer Immunoglobulin-Like Receptor 2DS2 (KIR2DS2), KIR2DL2-HLA-C1, and KIR2DL3 as Genetic Markers for Stratifying the Risk of Cytomegalovirus Infection in Kidney Transplant Recipients. International journal of molecular sciences 20 30696053
2004 Investigation of killer cell immunoglobulin-like receptor gene diversity III. KIR2DL3. Tissue antigens 17 15245374
2019 Differential contribution of education through KIR2DL1, KIR2DL3, and KIR3DL1 to antibody-dependent (AD) NK cell activation and ADCC. Journal of leukocyte biology 15 30698860
2014 Conjunctival scarring in trachoma is associated with the HLA-C ligand of KIR and is exacerbated by heterozygosity at KIR2DL2/KIR2DL3. PLoS neglected tropical diseases 15 24651768
2004 Differential expression of KIR/NKAT2 and CD94 molecules on decidual and peripheral blood CD56bright and CD56dim natural killer cell subsets. Fertility and sterility 15 15019821
2004 Isolation of a novel KIR2DL3-specific mAb: comparative analysis of the surface distribution and function of KIR2DL2, KIR2DL3 and KIR2DS2. International immunology 13 15314042
2010 Identification of four novel KIR2DL2 alleles and two novel KIR2DL3 alleles in an East African population. Human immunology 10 20875478
2015 The role of KIR2DL3/HLA-C*0802 in Brazilian patients with rheumatoid vasculitis. Clinics (Sao Paulo, Brazil) 9 26106958
2019 A novel antibody combination to identify KIR2DS2high natural killer cells in KIR2DL3/L2/S2 heterozygous donors. HLA 7 30381896
2022 Antiviral prophylaxis, male sex, and killer immunoglobulin-like receptor KIR2DL3 as markers for stratifying the risk of BK polyomavirus-associated nephropathy in kidney transplant recipients. Polish archives of internal medicine 5 36018060
2016 NK Cells Expressing the Inhibitory Killer Immunoglobulin-Like Receptors (iKIR) KIR2DL1, KIR2DL3 and KIR3DL1 Are Less Likely to Be CD16+ than Their iKIR Negative Counterparts. PloS one 5 27732638
2022 Clinical Impact of KIR2DS3 and KIR2DL3 Genes in Neuroblastoma Patients. Medical principles and practice : international journal of the Kuwait University, Health Science Centre 4 35537400
2021 Deciphering the biology of KIR2DL3+ T lymphocytes that are associated to relapse in haploidentical HSCT. Scientific reports 4 34349169
2016 The differential impact of natural killer (NK) cell education via KIR2DL3 and KIR3DL1 on CCL4 secretion in the context of in-vitro HIV infection. Clinical and experimental immunology 4 27506421
2016 A multifaceted computational report on the variants effect on KIR2DL3 and IFNL3 candidate gene in HCV clearance. Molecular biology reports 3 27461217
2010 Expression of KIR2DL3 and KIR2DS2 natural killer receptors in exercise. Bulletin of experimental biology and medicine 2 21165439
2024 The novel KIR2DL3*037 allele, identified by Sanger dideoxy nucleotide sequencing in a Chinese individual. HLA 1 38837624
2015 Investigation of killer cell immunoglobulin-like receptors KIR2DL2 and KIR2DL3 diversity and identification of ten novel KIR2DL3 alleles in the Chinese Han population. Scandinavian journal of immunology 1 25651940
2024 A single nucleotide substitution in exon 5 generated the novel KIR2DL3*00112 allele. HLA 0 38837671
2024 Discovery of the novel KIR2DL3*00111 allele in a Chinese Han individual. HLA 0 38887878
2015 A novel KIR2DL3 variant allele, KIR2DL3*032, which has arisen by a missense mutation in codon 231. Tissue antigens 0 25626612
2014 Characterization of the novel KIR2DL3*029 allele identified in a southern Chinese Han individual. Tissue antigens 0 24849728
2014 A novel KIR2DL3*00110 allele identified in a southern Chinese Han individual. Tissue antigens 0 24903265
2014 A novel KIR2DL3 variant allele, KIR2DL3*031, identified from a southern Chinese Han individual. Tissue antigens 0 25113143
2014 Identification of the novel KIR2DL3*030 allele from a southern Chinese Han individual. Tissue antigens 0 25131705
2014 The novel KIR2DL3*025 allele identified in an individual from a southern Chinese Han population. Tissue antigens 0 25155234
2014 A novel KIR2DL3 allele, KIR2DL3*026, found in an individual from a southern Chinese Han population. Tissue antigens 0 25346343
2014 A novel KIR2DL3 allele, KIR2DL3*027, identified in an individual from a southern Chinese Han population. Tissue antigens 0 25352250
2009 [KIR-NKAT2 expression and monocytoid dendritic cells transformation in children diagnosed for immune deficiency: a pilot study]. Medycyna wieku rozwojowego 0 19648663

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