Affinage

KIR2DL2

Killer cell immunoglobulin-like receptor 2DL2 · UniProt P43627

Length
348 aa
Mass
38.5 kDa
Annotated
2026-04-28
81 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIR2DL2 is an inhibitory killer-cell immunoglobulin-like receptor on NK cells that suppresses cytotoxicity upon engagement of HLA class I ligands, functioning as a key checkpoint in innate immune surveillance of virally infected and transformed cells. Its extracellular D1–D2 domains adopt a K-type Ig fold with a characteristic ~80° interdomain hinge angle; polymorphic residues at positions 16, 148, 11, and 35 tune this hinge geometry and confer higher binding avidity than the related KIR2DL3, enabling recognition of all C1-group HLA-C allotypes plus cross-reactivity with several C2-group HLA-C and HLA-B allotypes (PMID:10097129, PMID:18322206, PMID:23686481, PMID:40749828). Upon HLA-C engagement, KIR2DL2 is phosphorylated and recruits SHP-1/SHP-2, leading to dephosphorylation of PLCγ1 and suppression of NK cell activation independently of p56(lck); this inhibition dominates over co-expressed activating KIR2DS2 on the same cell (PMID:11750651, PMID:24078689). The peptide cargo presented by HLA-C fine-tunes KIR2DL2 binding strength, and HIV-1 and Lassa virus exploit this peptide-dependent recognition to select epitopes that enhance inhibitory KIR2DL2 engagement and evade NK cell killing (PMID:22807681, PMID:30711514, PMID:41198628).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1999 High

    Determining the three-dimensional structure of the KIR2DL2 extracellular domains established the K-type Ig fold topology, a distinctive ~80° interdomain hinge angle, and a putative ligand-binding site with charge complementarity to HLA-C, providing the first atomic framework for understanding inhibitory KIR recognition.

    Evidence X-ray crystallography of KIR2DL2 D1–D2 in two independent crystal forms at 2.9–3.0 Å

    PMID:10097129

    Open questions at the time
    • No complex structure with HLA-C ligand at this stage
    • Role of individual residues in ligand contact not yet tested by mutagenesis
  2. 2002 High

    Reconstitution of KIR2DL2 signaling in lck-negative cells demonstrated that ligand engagement triggers receptor phosphorylation, SHP-1/SHP-2 recruitment, and PLCγ1 dephosphorylation, establishing the proximal inhibitory signaling cascade independently of Src-family kinase p56(lck).

    Evidence Transfection of KIR2DL2 into p56(lck)-negative YT-Indy cells; pervanadate-stimulated phosphorylation, co-immunoprecipitation of SHP-1/SHP-2, cytotoxicity and PLCγ1 phosphorylation assays

    PMID:11750651

    Open questions at the time
    • Identity of the kinase that phosphorylates KIR2DL2 ITIMs in the absence of lck remains undefined
    • Downstream substrates beyond PLCγ1 not characterized
  3. 2008 High

    Systematic binding analysis across 93 HLA isoforms revealed that KIR2DL2 recognizes all C1-group and several C2-group HLA-C allotypes plus HLA-B*4601 and HLA-B*7301, and site-directed mutagenesis pinpointed residues Arg16 and Cys148 near the interdomain hinge as determinants of higher avidity relative to KIR2DL3.

    Evidence Recombinant KIR extracellular domain binding assays to 93 HLA isoforms; site-directed mutagenesis of positions 16 and 148

    PMID:18322206

    Open questions at the time
    • Structural basis for cross-reactivity with HLA-B allotypes not resolved
    • How hinge angle change translates to altered binding kinetics not quantified by SPR in this study
  4. 2012 High

    Discovery that HLA-C-presented HIV-1 Gag peptides modulate KIR2DL2 binding and NK cell inhibition established a peptide-dependent mechanism of viral immune evasion, showing that the peptide cargo is not merely a passenger but an active determinant of inhibitory KIR engagement.

    Evidence KIR2DL2-Fc binding assays, HLA stabilization assays, and primary NK cell degranulation assays with variant Gag peptides

    PMID:22807681

    Open questions at the time
    • Structural basis for peptide discrimination not yet determined at atomic resolution
    • In vivo selection pressure on viral peptides not demonstrated
  5. 2013 High

    Functional and mutagenesis studies showed that allele-specific residues at positions 11 and 35 (distal to the HLA-C contact surface) modulate KIR2DL2/L3 binding avidity by altering the interdomain hinge angle, and that KIR2DL2-mediated inhibition dominates over co-expressed KIR2DS2 activation, establishing KIR2DL2 as the functionally dominant receptor in NK cells bearing both.

    Evidence SPR binding, flow cytometry, mutagenesis, IFN-γ inhibition in KHYG-1 cells; NK clone reactivity assays across HLA-C panels

    PMID:23686481 PMID:24078689

    Open questions at the time
    • Crystal structure confirming hinge angle change from positions 11/35 not available at this time
    • Mechanism by which inhibitory signal overrides activating KIR2DS2 at the signalosome level is undefined
  6. 2014 Medium

    Extending the peptide-dependent evasion paradigm, additional HIV-1 Gag epitopes presented by HLA-C*03:04 were shown to promote KIR2DL2 binding and NK inhibition, and KIR2DL2+ NK cells were found to be less sensitive than KIR2DL3+ cells to peptide repertoire changes owing to their higher avidity, linking receptor strength to functional tuning of peptide discrimination.

    Evidence KIR2DL2-Fc binding and NK degranulation assays with defined peptides; mathematical modeling of inhibitory thresholds

    PMID:24785948 PMID:25359276

    Open questions at the time
    • Whether higher avidity uniformly reduces sensitivity to all peptide variants or is context-dependent remains untested
    • No in vivo data confirming differential peptide sensitivity between KIR2DL2 and KIR2DL3
  7. 2016 Medium

    Position-35 polymorphism (E35 vs Q35) was shown to modulate NK cytotoxicity and licensing strength, and KIR2DL2 expression was linked to skewing of NK cytokine secretion toward a Th17 profile during herpesvirus infection, expanding the functional consequences of KIR2DL2 signaling beyond degranulation.

    Evidence NK cytotoxicity assays with allelic dissection and molecular modeling; in vitro HSV-1 infection with cytokine profiling of KIR2DL2+ vs KIR2DL2− NK subsets

    PMID:27030405 PMID:27138091

    Open questions at the time
    • E35-H55 interaction predicted by modeling lacks crystallographic validation
    • Th17 skewing mechanism downstream of ITIM signaling is uncharacterized
  8. 2018 Medium

    Demonstration that decitabine upregulates KIR2DL2/3 transcription by demethylating the promoter and enabling Sp-1 binding revealed an epigenetic mechanism controlling KIR2DL2 expression and consequent inhibition of γδ T cell cytotoxicity.

    Evidence Flow cytometry, promoter methylation analysis, Sp-1 binding assay, and cytotoxicity assays in γδ T cells treated with decitabine

    PMID:29632540

    Open questions at the time
    • Whether this epigenetic regulation operates identically in conventional NK cells is untested
    • Chromatin accessibility or histone modification data not provided
  9. 2019 Medium

    Lassa virus-derived peptides presented by HLA-C were shown to strongly inhibit KIR2DL2+ NK degranulation, extending the peptide-dependent evasion mechanism beyond HIV-1 and indicating it is a general viral strategy exploiting the HLA-C/KIR2DL2 axis.

    Evidence Peptide-HLA stabilization, KIR2DL2 binding, and NK polyfunction degranulation assays with LASV NP and GP peptides

    PMID:30711514

    Open questions at the time
    • No crystal structure of KIR2DL2 with LASV peptide-HLA complex
    • In vivo relevance in Lassa fever patients not examined
  10. 2021 High

    Crystal structures of KIR2DL2 and KIR2DL3 bound to HLA-C*07:02 revealed distinct docking modalities, explaining their differential recognition of C1 allotypes at atomic resolution, and in vivo HIV-1 sequence data showed that clade C virus avoids mutations that would abolish KIR2DL2 binding, confirming peptide-dependent NK evasion under physiological selection pressure.

    Evidence X-ray crystallography of KIR2DL2/HLA-C*07:02 complex with mutagenesis and primary NK assays; HIV-1 clade C sequence analysis combined with KIR2DL2-Fc binding and disinhibition assays

    PMID:33273184 PMID:33846289

    Open questions at the time
    • Full energetic decomposition of docking modality differences not performed
    • Whether KIR2DL2 docking differences extend to all C1 allotypes or are HLA-C*07:02-specific is not resolved
  11. 2025 High

    Crystal structures of KIR2DL2 with HLA-B*73:01 and with HLA-C*12:02 presenting HIV-derived escape-mutant peptides provided the structural basis for KIR2DL2 cross-reactivity with non-HLA-C ligands and for peptide-dependent modulation of inhibitory engagement, unifying the molecular mechanism of viral immune evasion at atomic resolution.

    Evidence X-ray crystallography of KIR2DL2/HLA-B*73:01 and KIR2DL2/HLA-C*12:02-peptide complexes; mass spectrometry immunopeptidomics of HIV-1-infected cells; NK functional assays

    PMID:40749828 PMID:41198628

    Open questions at the time
    • Whether KIR2DL2 engages other HLA-B allotypes (e.g., B*46:01) with the same docking mode is untested
    • Immunopeptidome data are from cell lines and may not fully recapitulate in vivo peptide presentation

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the kinase(s) that phosphorylate KIR2DL2 ITIMs, the structural basis for dominance of KIR2DL2 inhibition over KIR2DS2 activation at the signalosome level, and whether peptide-dependent evasion by non-HIV/non-LASV viruses and tumors is a general phenomenon.
  • ITIM kinase identity unknown
  • Signalosome-level mechanism of inhibitory dominance over KIR2DS2 not resolved
  • Breadth of peptide-dependent evasion across diverse pathogens and cancer untested

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
Localization
GO:0005886 plasma membrane 3
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 2
Partners
HLA-CKIR2DS2PLCG1PTPN11PTPN6

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Crystal structure of KIR2DL2 extracellular ligand-binding domains determined at 2.9–3.0 Å resolution, revealing K-type Ig topology with cis-proline residues in both domains, a hinge angle of ~80° (14° larger than KIR2DL1), and a putative ligand-binding site formed by variable loop residues with charge distribution complementary to HLA-C. X-ray crystallography (orthorhombic and trigonal crystal forms) Proceedings of the National Academy of Sciences of the United States of America High 10097129
2008 KIR2DL2 binds all C1 HLA-C allotypes and also cross-reacts with several C2 allotypes (e.g., Cw*0501, Cw*0202) and two HLA-B allotypes (B*4601, B*7301); it is a stronger receptor than KIR2DL3. Site-directed mutagenesis showed that the combination of arginine at position 16 (D1) and cysteine at position 148 (D2) — residues near the flexible D1–D2 hinge — is required for the higher avidity of KIR2DL2 over KIR2DL3, suggesting these polymorphisms alter the interdomain hinge angle and ligand-binding site orientation. Binding assays to 93 HLA isoforms, site-directed mutagenesis of recombinant KIR extracellular domains, functional analysis Journal of immunology (Baltimore, Md. : 1950) High 18322206
2002 KIR2DL2 inhibits CD28-mediated natural cytotoxicity in a p56(lck)-independent manner. Upon HLA-Cw3 engagement, KIR2DL2 undergoes phosphorylation, recruits SHP1/SHP2, and reduces CD28-induced tyrosine phosphorylation of PLC-γ1, indicating that PLC-γ1 dephosphorylation mediates KIR2DL2's inhibitory signal. Transfection of p56(lck)-negative YT-Indy cells with KIR2DL2, pervanadate-stimulated phosphorylation assays, co-immunoprecipitation of SHP1/SHP2, cytotoxicity assays with blocking antibodies, PLC-γ1 phosphorylation analysis Molecular immunology High 11750651
2021 Crystal structures of KIR2DL2 and KIR2DL3 in complex with HLA-C*07:02 reveal that KIR2DL2 adopts a different docking modality over HLA-C*07:02 compared to KIR2DL3. Mutagenesis confirmed differences in the mechanism of HLA-C1 allotype recognition, and KIR2DL2's binding geometry combines with KIR2DS2 activity to distinguish functional HLA-C1 recognition. X-ray crystallography of KIR/HLA complexes, site-directed mutagenesis, primary NK cell activation assays Nature communications High 33846289
2013 KIR2DL3*005, a KIR2DL3 allele bearing arginine at residue 11 and glutamic acid at residue 35, binds HLA-C with affinity and avidity comparable to KIR2DL2*001. Site-directed mutagenesis established that the combination of these two residues (distal to the KIR/HLA-C interface) is critical, likely by altering the interdomain hinge angle toward that of KIR2DL2*001. Surface plasmon resonance, KIR binding to HLA panel, flow cytometry, site-directed mutagenesis, molecular modeling, IFN-γ inhibition assay in KHYG-1 NK cells Journal of immunology (Baltimore, Md. : 1950) High 23686481
2012 HIV-1 p24 Gag peptide Gag209-218 (AAEWDRLHPV) presented by HLA-Cw*0102 allows binding of KIR2DL2 and leads to significant inhibition of KIR2DL2+ primary NK cells; sequence variations at position 7 of this epitope modulate KIR2DL2 binding, identifying a peptide-dependent mechanism by which HIV-1 could escape NK cell surveillance. KIR2DL2-IgG fusion protein binding assays, flow cytometry-based HLA stabilization assay, NK cell degranulation assays PLoS pathogens High 22807681
2013 KIR2DL2+ NK cells recognize a broader spectrum of HLA-C allotypes (both C1 and C2) than KIR2DL1+ NK cells. When KIR2DL2 and KIR2DS2 are co-expressed, KIR2DL2-mediated inhibition overrides KIR2DS2-mediated activation, demonstrating a dominant inhibitory function of KIR2DL2 in the KIR2D repertoire. NK cell reactivity assays against HLA-C+ target cells, NK cell clone analysis, KIR co-expression functional assays Journal of immunology (Baltimore, Md. : 1950) High 24078689
2004 KIR2DL2 and KIR2DL3 can be distinguished at the serological and functional levels using novel mAb ECM41 (KIR2DL3-specific) in combination with GL183 (cross-reactive). NK cell clones expressing KIR2DL3 or KIR2DL2 (previously serologically indistinguishable) were shown to differ in HLA class I specificity. Simultaneous engagement of KIR2DL3 and KIR2DS2 in co-expressing NK clones was analyzed in redirected killing assays. Generation of KIR2DL3-specific monoclonal antibody ECM41, cell transfectants, flow cytometry, NK clone redirected killing assays International immunology Medium 15314042
2014 HLA-C*03:04-restricted HIV-1 p24 Gag epitopes Gag144-152, Gag163-171, and Gag295-304 enable KIR2DL2 binding to HLA-C*03:04 and inhibit KIR2DL2+ primary NK cells; naturally occurring minor variants of Gag295-304 enhance KIR2DL2 binding, showing that peptide sequence variations modulate inhibitory KIR engagement. KIR2DL2-Fc construct binding assays, HLA stabilization assays, NK cell degranulation assays AIDS (London, England) Medium 24785948
2016 KIR2DL2+ NK cells suppress HIV-1 replication in HLA-C*14:03+ or HLA-C*12:02+ cells more effectively than KIR2DL2- NK cells. The mechanism involves reduced expression of peptide-HLA complexes on the cell surface (reduced KIR2DL2 ligand availability) rather than altered KIR2DL2 binding affinity to pHLA. In vitro viral suppression assays, KIR2DL2+ vs KIR2DL2- NK cell functional comparison, binding affinity measurements Cell reports Medium 27880898
2016 KIR2DL2/L3 alleles with glutamic acid at position 35 (E35) are functionally stronger (greater NK cell cytotoxicity and licensing) than those with glutamine at the same position (Q35). Molecular modeling indicates E35 interacts with histidine at position 55, stabilizing the KIR2DL2/L3 dimer and reducing entropy loss upon HLA-C ligand binding. NK cell cytotoxicity assays, molecular modeling Scientific reports Medium 27030405
2014 KIR2DL2+ NK cells are less sensitive to changes in the peptide content of HLA-C class I than KIR2DL3+ NK cells. Specifically, KIR2DL3+ NK cells are more readily activated by weak inhibitory (VAPWNSRAL) and antagonist (VAPWNSDAL) peptides, indicating that stronger KIR2DL2 avidity for HLA-C/peptide complexes reduces NK cell sensitivity to peptide repertoire variation. NK cell degranulation assays with defined inhibitory, weak inhibitory, and antagonist peptides; mathematical modeling European journal of immunology Medium 25359276
2018 Decitabine (a DNA methyltransferase inhibitor) upregulates KIR2DL2/3 expression in KIR2DL2/3-negative γδ T cells by inhibiting KIR2DL2/3 promoter methylation, which enhances Sp-1 binding to the KIR2DL2/3 promoter and activates gene expression, resulting in reduced cytotoxicity of these cells. Flow cytometry, promoter methylation analysis, Sp-1 binding assay, cytotoxicity assays Frontiers in immunology Medium 29632540
2025 Crystal structure of KIR2DL2 in complex with HLA-B*73:01 (a non-HLA-C ligand) reveals differences in the binding interface compared to previously solved KIR2DL2/HLA-C complex structures. Mass spectrometry-based immunopeptidome profiling of HIV-1-infected cells and KIR2DL2-HLA-C*12:02-peptide crystal structures demonstrate the molecular basis for KIR2DL2 recognition of escape mutant epitopes selected by CD8+ T cells. X-ray crystallography (KIR2DL2/HLA-C*12:02-peptide and KIR2DL2/HLA-B*73:01), mass spectrometry immunopeptidomics, NK cell functional assays Nature communications High 41198628
2024 Crystal structure of KIR2DL2 in complex with HLA-B*73:01 reveals that KIR2DL2 engages this non-HLA-C molecule with differences from previously solved HLA-C complexes, providing structural evidence that KIR2DL2 can recognize HLA-B allotypes in addition to HLA-C. X-ray crystallography The Journal of biological chemistry High 40749828
2012 In multiple sclerosis patients, CpG treatment caused NK cells to upregulate KIR2DL2 and show decreased degranulation and cytotoxicity in response to HSV-1 infection. Direct CpG treatment of purified NK cells reproduced KIR2DL2 upregulation, indicating a cell-autonomous mechanism linking TLR9 pathway activation to increased inhibitory KIR2DL2 expression and impaired NK cell function. In vitro viral infection assays, cytokine secretion, NK cell activation and degranulation assays, KIR expression measurement by flow cytometry on purified NK cells Journal of neuroimmunology Medium 22871633
2016 MS patients with KIR2DL2+ NK cells that fail to control HSV-1 infection produce high levels of Th17 cytokines (rather than IFN-γ), while KIR2DL2- NK cells from MS patients release Th1 cytokines (IFN-γ). This demonstrates that KIR2DL2 inhibitory signaling skews NK cell cytokine secretion toward a Th17 profile during herpesvirus infection. In vitro HSV-1 infection assays, cytokine secretion analysis by flow cytometry/ELISA in KIR2DL2+ vs. KIR2DL2- NK cell subsets Journal of neuroimmunology Medium 27138091
2019 Lassa virus (LASV) NP and GP-derived peptides presented by HLA-C molecules (but not HLA-B or HLA-A) strongly inhibit degranulation of KIR2DL2+ NK cells. A specific variant of glycoprotein epitope vGP420 significantly increases this inhibitory effect, suggesting LASV exploits the HLA-C/KIR2DL2 axis to escape NK cell killing. In silico peptide screening, peptide-HLA stabilization assays, KIR2DL2 binding assays, NK cell degranulation polyfunction assays EBioMedicine Medium 30711514
2021 HIV-1 clade C avoids acquiring a p24 Gag mutation that would abolish KIR2DL2 binding to HLA-C*03:04, demonstrating in vivo selection pressure to maintain KIR2DL2-mediated NK inhibition in individuals with the KIR2DL2+/HLA-C*03:04+ genotype. HIV-1 sequence analysis in KIR2DL2+/HLA-C*03:04+ individuals, KIR2DL2-Fc binding assays, NK cell disinhibition assays AIDS (London, England) Medium 33273184

Source papers

Stage 0 corpus · 81 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
2001 Human natural killer cells with polyclonal lectin and immunoglobulinlike receptors develop from single hematopoietic stem cells with preferential expression of NKG2A and KIR2DL2/L3/S2. Blood 164 11468170
2004 CD158k/KIR3DL2 is a new phenotypic marker of Sezary cells: relevance for the diagnosis and follow-up of Sezary syndrome. The Journal of investigative dermatology 106 15086570
1999 Crystal structure of the HLA-Cw3 allotype-specific killer cell inhibitory receptor KIR2DL2. Proceedings of the National Academy of Sciences of the United States of America 98 10097129
2012 Diverse functionality among human NK cell receptors for the C1 epitope of HLA-C: KIR2DS2, KIR2DL2, and KIR2DL3. Frontiers in immunology 92 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
1993 Purification and characterization of a bovine serum lectin (CL-43) with structural homology to conglutinin and SP-D and carbohydrate specificity similar to mannan-binding protein. The Journal of biological chemistry 84 8486682
2011 KIR2DL2 enhances protective and detrimental HLA class I-mediated immunity in chronic viral infection. PLoS pathogens 66 22022261
2013 Allelic variation in KIR2DL3 generates a KIR2DL2-like receptor with increased binding to its HLA-C ligand. Journal of immunology (Baltimore, Md. : 1950) 60 23686481
2012 HLA-Cw*0102-restricted HIV-1 p24 epitope variants can modulate the binding of the inhibitory KIR2DL2 receptor and primary NK cell function. PLoS pathogens 59 22807681
2010 Natural-killer cell amplification for adoptive leukemia relapse immunotherapy: comparison of three cytokines, IL-2, IL-15, or IL-7 and impact on NKG2D, KIR2DL1, and KIR2DL2 expression. Experimental hematology 56 20172016
2008 CD158k/KIR3DL2 is a useful marker for identifying neoplastic T-cells in Sézary syndrome by flow cytometry. Cytometry. Part B, Clinical cytometry 53 18061949
2014 CD158k is a reliable marker for diagnosis of Sézary syndrome and reveals an unprecedented heterogeneity of circulating malignant cells. The Journal of investigative dermatology 51 25158034
2009 Killer immunoglobulin-like receptors (KIR2DL2 and/or KIR2DS2) in presence of their ligand (HLA-C1 group) protect against chronic myeloid leukaemia. Tissue antigens 50 19493232
2021 Structural plasticity of KIR2DL2 and KIR2DL3 enables altered docking geometries atop HLA-C. Nature communications 45 33846289
2012 Altered natural killer cells' response to herpes virus infection in multiple sclerosis involves KIR2DL2 expression. Journal of neuroimmunology 43 22871633
1994 Primary structure of bovine collectin-43 (CL-43). Comparison with conglutinin and lung surfactant protein-D. The Journal of biological chemistry 41 8163480
2014 Sequence variations in HIV-1 p24 Gag-derived epitopes can alter binding of KIR2DL2 to HLA-C*03:04 and modulate primary natural killer cell function. AIDS (London, England) 37 24785948
2007 Influence of KIR gene diversity on the course of HSV-1 infection: resistance to the disease is associated with the absence of KIR2DL2 and KIR2DS2. Tissue antigens 37 17559579
2007 CD158K/KIR3DL2 transcript detection in lesional skin of patients with erythroderma is a tool for the diagnosis of Sézary syndrome. The Journal of investigative dermatology 35 17703174
2002 Lung surfactant protein D (SP-D) and the molecular diverted descendants: conglutinin, CL-43 and CL-46. Immunobiology 34 12396011
2021 Natural Killer Cells Generated From Human Induced Pluripotent Stem Cells Mature to CD56brightCD16+NKp80+/-In-Vitro and Express KIR2DL2/DL3 and KIR3DL1. Frontiers in immunology 32 34017328
2012 CD158k/KIR3DL2 and NKp46 are frequently expressed in transformed mycosis fungoides. Experimental dermatology 32 22621189
2009 Absolute CD3+ CD158k+ lymphocyte count is reliable and more sensitive than cytomorphology to evaluate blood tumour burden in Sézary syndrome. The British journal of dermatology 31 19681856
2019 KIR2DS2/KIR2DL2/HLA-C1 Haplotype Is Associated with Alzheimer's Disease: Implication for the Role of Herpesvirus Infections. Journal of Alzheimer's disease : JAD 30 30689576
2012 KIR2DL2/S2 and HLA-C C1C1 genotype is associated with better response to treatment and prolonged survival of patients with non-small cell lung cancer in a Polish Caucasian population. Human immunology 30 22836042
2016 HIV-1 Control by NK Cells via Reduced Interaction between KIR2DL2 and HLA-C∗12:02/C∗14:03. Cell reports 29 27880898
2014 Peptide selectivity discriminates NK cells from KIR2DL2- and KIR2DL3-positive individuals. European journal of immunology 28 25359276
2016 KIR3DL2 (CD158k) is a potential therapeutic target in primary cutaneous anaplastic large-cell lymphoma. The British journal of dermatology 27 27037558
2011 Enrichment of variations in KIR3DL1/S1 and KIR2DL2/L3 among H1N1/09 ICU patients: an exploratory study. PloS one 26 22216211
2004 The genes encoding bovine SP-A, SP-D, MBL-A, conglutinin, CL-43 and CL-46 form a distinct collectin locus on Bos taurus chromosome 28 (BTA28) at position q.1.8-1.9. Animal genetics 21 15265076
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
2018 Decitabine Inhibits Gamma Delta T Cell Cytotoxicity by Promoting KIR2DL2/3 Expression. Frontiers in immunology 20 29632540
2019 Follicular lymphoma patients with KIR2DL2 and KIR3DL1 and their ligands (HLA-C1 and HLA-Bw4) show improved outcome when receiving rituximab. Journal for immunotherapy of cancer 17 30871628
2009 Lack of killer immunoglobulin-like receptor 2DS2 (KIR2DS2) and KIR2DL2 is associated with poor responses to therapy of recurrent hepatitis C virus in liver transplant recipients. Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society 17 19877200
2020 Decreased HLA-C1 alleles in couples of KIR2DL2 positive women with recurrent pregnancy loss. Journal of reproductive immunology 16 32846355
2019 HLA-C-restricted viral epitopes are associated with an escape mechanism from KIR2DL2+ NK cells in Lassa virus infection. EBioMedicine 15 30711514
2016 KIR2DL2/2DL3-E(35) alleles are functionally stronger than -Q(35) alleles. Scientific reports 15 27030405
2016 KIR2DL2 and KIR2DS2 as genetic markers to the methotrexate response in rheumatoid arthritis patients. Immunopharmacology and immunotoxicology 15 27251940
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
2018 KIR2DL2 combined with HLA-C1 confers risk of hepatitis C virus-related hepatocellular carcinoma in younger patients. Oncotarget 14 29731972
2016 KIR2DL2 inhibitory pathway enhances Th17 cytokine secretion by NK cells in response to herpesvirus infection in multiple sclerosis patients. Journal of neuroimmunology 14 27138091
2006 Conglutinin, CL-43 and CL-46--three bovine collectins. Polish journal of veterinary sciences 14 17203746
2014 Diversity of killer cell immunoglobulin-like receptor (KIR) genotypes and KIR2DL2/3 variants in HCV treatment outcome. PloS one 13 24927414
2009 Association of KIR2DL2 polymorphism rs2756923 with type 1 diabetes and preliminary evidence for lack of inhibition through HLA-C1 ligand binding. Tissue antigens 13 19392800
2006 Influence of interleukin IL-2 and IL-12 + IL-18 on surface expression of immunoglobulin-like receptors KIR2DL1, KIR2DL2, and KIR3DL2 in natural killer cells. Mediators of inflammation 13 17047292
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
2022 The KIR2DL2/HLA-C1C1 Gene Pairing Is Associated With an Increased Risk of SARS-CoV-2 Infection. Frontiers in immunology 12 35874712
2015 Increased frequencies of the killer immunoglobulin-like receptor genes KIR2DL2 and KIR2DS2 are associated with neuroblastoma. Tissue antigens 12 26202659
2014 Evaluation of the implication of KIR2DL2 receptor in multiple sclerosis and herpesvirus susceptibility. Journal of neuroimmunology 12 24735502
2008 Investigation of killer cell immunoglobulin-like receptor (KIR) gene diversity: KIR2DL2, KIR2DL5 and KIR2DS5. Tissue antigens 12 18498296
2021 Large-Scale Imputation of KIR Copy Number and HLA Alleles in North American and European Psoriasis Case-Control Cohorts Reveals Association of Inhibitory KIR2DL2 With Psoriasis. Frontiers in immunology 11 34177931
2014 Membrane expression of NK receptors CD160 and CD158k contributes to delineate a unique CD4+ T-lymphocyte subset in normal and mycosis fungoides skin. Cytometry. Part A : the journal of the International Society for Analytical Cytology 11 25044837
2010 Identification of four novel KIR2DL2 alleles and two novel KIR2DL3 alleles in an East African population. Human immunology 10 20875478
1993 The genomics of soluble proteins with collagenous domains: C1q, MBL, SP-A, SP-D, conglutinin, and CL-43. Behring Institute Mitteilungen 10 8172588
2022 CD158k and PD-1 expressions define heterogeneous subtypes of Sezary syndrome. Blood advances 9 34570200
2022 The Interaction of HLA-C1/KIR2DL2/L3 Promoted KIR2DL2/L3 Single-Positive/NKG2C-Positive Natural Killer Cell Reconstitution, Raising the Incidence of aGVHD after Hematopoietic Stem Cell Transplantation. Frontiers in immunology 9 35572602
2003 Genomic and molecular characterization of CL-43 and its proximal promoter. Biochimica et biophysica acta 9 12527419
2002 Inhibition of CD28-mediated natural cytotoxicity by KIR2DL2 does not require p56(lck) in the NK cell line YT-Indy. Molecular immunology 9 11750651
2020 Inhibitory KIR2DL2 Gene: Risk for Deep Endometriosis in Euro-descendants. Reproductive sciences (Thousand Oaks, Calif.) 8 32661880
2016 KIR Gene Content Diversity in a Zimbabwean Population: Does KIR2DL2 Have a Role in Protection Against Human Immunodeficiency Virus Infection? Omics : a journal of integrative biology 8 27930093
2019 KIR2DS4, KIR2DL2, and KIR2DS4del are linked with basaloid tumors, lymph node metastasis, advanced stage and metastatic risk in head and neck squamous cell carcinoma. Experimental and molecular pathology 6 31751561
2022 Herpesvirus Infections in KIR2DL2-Positive Multiple Sclerosis Patients: Mechanisms Triggering Autoimmunity. Microorganisms 5 35336070
2021 Increased Susceptibility of the CD57- NK Cells Expressing KIR2DL2/3 and NKG2C to iCasp9 Gene Retroviral Transduction and the Relationships with Proliferative Potential, Activation Degree, and Death Induction Response. International journal of molecular sciences 5 34948123
2019 KIR2DL2/S2 and KIR2DS5 in alcoholic cirrhotic patients undergoing liver transplantation. Archives of medical science : AMS 5 34025847
2024 KIR2DL2/DL3+NKs and Helios+Tregs in Peripheral Blood Predict Nivolumab Response in Patients with Metastatic Renal Cell Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 3 39167621
2019 Association of KIR2DL2 gene with anti-cyclic citrullinated protein antibodies for serodiagnosis in rheumatoid arthritis. Medicina 3 31284249
2002 Novel characterisation of the gene encoding conglutinin reveals that previously characterised promoter corresponds to the CL-43 promoter. Molecular immunology 3 12213326
2022 Inhibitory KIR2DL2 receptor and HHV-8 in classic or endemic Kaposi sarcoma. Clinical and experimental medicine 2 35169985
2015 Allelic polymorphism of KIR2DL2/2DL3 in a southern Chinese population. Tissue antigens 2 26423800
2025 Molecular characterization of the archaic HLA-B∗73:01 allele reveals presentation of a unique peptidome and skewed engagement by KIR2DL2. The Journal of biological chemistry 1 40749828
2024 Day 100 Recovery of Absolute Number of Inhibitory KIR2DL2 and Activating NKp30 Natural Killer Cells Predicts Survival Post-Autologous Stem Cell Transplantation in Lymphomas. Biomedicines 1 39200272
2021 HIV-1 evades a Gag mutation that abrogates killer cell immunoglobulin-like receptor binding and disinhibits natural killer cells in infected individuals with KIR2DL2+/HLA-C*03: 04+ genotype. AIDS (London, England) 1 33273184
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
2026 SARS-CoV-2 Infection Associated with HHV-6A Reactivation and an Inhibitory KIR2DL2/HLA-C1 Immunogenetic Profile. Microorganisms 0 41597753
2025 Molecular basis for selection and inhibition of HIV-1 escape virus by T cells and KIR2DL2+NK cells. Nature communications 0 41198628
2024 Molecular characterization of the archaic HLA-B*73:01 allele reveals presentation of a unique peptidome and skewed engagement by KIR2DL2. bioRxiv : the preprint server for biology 0 39651149
2023 Presence of KIR2DL2/S2, KIR2DL5, and KIR3DL1 Molecules in Liver Transplant Recipients with Alcoholic Cirrhosis Could Be Implicated in Death by Graft Failure. Diagnostics (Basel, Switzerland) 0 37046435
2021 [Use of the multiparametric panel CD3/CD4/CD8/CD7/CD26/CD158k in the detection and use of flow cytometry of Sezary cells]. Annales de biologie clinique 0 34165432
2018 Stable Frequencies of HLA-C*03:04/Peptide-Binding KIR2DL2/3+ Natural Killer Cells Following Vaccination. Frontiers in immunology 0 30386333
2018 HLA-C*18:01 and KIR2DL2+C1 genetic variants are associated with low viral load in cART naïve HIV-infected adult Zimbabweans. Journal of infection in developing countries 0 32027612