Recognition of HLA‐A3 and HLA‐A11 by KIR3DL2 is peptide‐specific

Hansasuta, Pokrath; Dong, Tao; Thananchai, Hathairat; Weekes, Michael P.; Willberg, Christian; Aldemir, Hatice; Rowland‐Jones, Sarah; Braud, Véronique M.

doi:10.1002/eji.200425089

Cited by 284 publications

(265 citation statements)

References 27 publications

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“…1A). This set of HLA class I allotypes retains the C1, C2, and Bw4 epitopes, the major ligands for inhibitory KIR (7), but lacks the A3/A11 epitope recognized by KIR3DL2 (21). During NK cell development, interactions between C1, C2, and Bw4 and cognate KIR determine the strength with which mature NK cells respond to cells whose HLA class I expression is perturbed by disease, a developmental process termed NK cell education (22).…”

Section: Resultsmentioning

confidence: 99%

“…During NK cell development, interactions between C1, C2, and Bw4 and cognate KIR determine the strength with which mature NK cells respond to cells whose HLA class I expression is perturbed by disease, a developmental process termed NK cell education (22). The A3/A11 epitope contributes little to NK cell education (23,24), a distinction that correlates with the exceptionally high sensitivity of KIR3DL2 to the peptide bound by HLA-A*03 or A*11 (21).…”

Section: Resultsmentioning

confidence: 99%

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Co-evolution of KIR2DL3 with HLA-C in a human population retaining minimal essential diversity of KIR and HLA class I ligands

Gendzekhadze

Norman

Abi-Rached

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

111

178

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Natural killer (NK) cells contribute to immunity and reproduction.Guiding these functions, and NK cell education, are killer cell Ig-like receptors (KIR), NK cell receptors that recognize HLA class I. In most human populations, these highly polymorphic receptors and ligands combine with extraordinary diversity. To assess how much of this diversity is necessary, we studied KIR and HLA class I at high resolution in the Yucpa, a small South Amerindian population that survived an approximate 15,000-year history of population bottleneck and epidemic infection, including recent viral hepatitis. The Yucpa retain the three major HLA epitopes recognized by KIR. Through balancing selection on a few divergent haplotypes the Yucpa maintain much of the KIR variation found worldwide. HLA-C*07, the strongest educator of C1-specific NK cells, has reached unusually high frequency in the Yucpa. Concomitantly, weaker variants of the C1 receptor, KIR2DL3, were selected and have largely replaced the form of KIR2DL3 brought by the original migrants from Asia. HLA-C1 and KIR2DL3 homozygosity has previously been correlated with resistance to viral hepatitis. Selection of weaker forms of KIR2DL3 in the Yucpa can be seen as compensation for the high frequency of the potent HLA-C*07 ligand. This study provides an estimate of the minimal KIR-HLA system essential for long-term survival of a human population. That it contains all functional elements of KIR diversity worldwide, attests to the competitive advantage it provides, not only for surviving epidemic infections, but also for rebuilding populations once infection has passed.Amerindian ͉ immune diversity ͉ natural selection ͉ NK cells ͉ reproduction

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Co-evolution of KIR2DL3 with HLA-C in a human population retaining minimal essential diversity of KIR and HLA class I ligands

Gendzekhadze

Norman

Abi-Rached

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

111

178

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“…Moreover, this study has, for the first time to our knowledge, mapped the association of MHC-I molecules with BD to specific HLA-B and HLA-A amino acid residues, most of which cluster in the antigen-binding groove at positions known to influence strongly the selection and binding of peptide antigens by MHC-I molecules. These findings have important implications for the pathophysiology of BD, because peptide binding by MHC-I directly affects (i) the folding and stability of peptide-MHC-I complexes, which in turn determine their surface expression vs. retention in the endoplasmic reticulum; (ii) the recognition of peptide-MHC-I complexes by antigen-specific Tcell receptors on CTLs; and (iii) the engagement of KIRs on CTLs and NK cells by peptide-MHC-I complexes (26)(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Behçet disease-associated MHC class I residues implicate antigen binding and regulation of cell-mediated cytotoxicity

Ombrello

Kirino

Bakker

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

128

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The HLA protein, HLA-B*51, encoded by HLA-B in MHC, is the strongest known genetic risk factor for Behçet disease (BD). Associations between BD and other factors within the MHC have been reported also, although strong regional linkage disequilibrium complicates their confident disentanglement from HLA-B*51. In the current study, we examined a combination of directly obtained and imputed MHC-region SNPs, directly obtained HLA-B locus types, and imputed classical HLA types with their corresponding polymorphic amino acid residues for association with BD in 1,190 cases and 1,257 controls. SNP mapping with logistic regression of the MHC identified the HLA-B/MICA region and the region between HLA-F and HLA-A as independently associated with BD (P < 1.7 × 10 −8 ). HLA-B*51, -A*03, -B*15, -B*27, -B*49, -B*57, and -A*26 each contributed independently to BD risk. We directly examined rs116799036, a noncoding SNP upstream of HLA-B that was recently suggested to underlie the association of HLA-B*51 with BD, but we were unable to replicate that finding in our collection. Instead, we mapped the BD association to seven MHC class I (MHC-I) amino acid residues, including anchor residues that critically define the selection and binding of peptides to MHC-I molecules, residues known to influence MHC-Ikiller immunoglobulin-like receptor interactions, and a residue located in the signal peptide of HLA-B. The locations of these variants collectively implicate MHC-I peptide binding in the pathophysiology of BD. Furthermore, several lines of evidence suggest a role for altered regulation of cellular cytotoxicity in BD pathogenesis.HLA imputation | autoinflammation | antigen presentation | killer immunoglobulin-like receptors | natural killer cells

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“…1C). The identity of the amino acid in position 8 of the peptide has been described to be critical for HLA/KIR binding [12][13][14], as confirmed by crystallization studies [18].…”

mentioning

confidence: 92%

“…While the concept of peptides modulating the interaction of specific KIRs and their HLA-A, B or C ligands is not new [12][13][14][15] Lunemann et al perform the first systematic screen for such peptides in HCV infection. Only very few HLA-C restricted peptides have been identified in HCV infection, even when one uses T cell activation rather than NK cell inhibition as a readout.…”

mentioning

confidence: 99%

Peptide-dependent HLA-KIR-mediated regulation of NK cell function

Rehermann

2016

Journal of Hepatology

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Recognition of HLA‐A3 and HLA‐A11 by KIR3DL2 is peptide‐specific

Cited by 284 publications

References 27 publications

Co-evolution of KIR2DL3 with HLA-C in a human population retaining minimal essential diversity of KIR and HLA class I ligands

Co-evolution of KIR2DL3 with HLA-C in a human population retaining minimal essential diversity of KIR and HLA class I ligands

Behçet disease-associated MHC class I residues implicate antigen binding and regulation of cell-mediated cytotoxicity

Peptide-dependent HLA-KIR-mediated regulation of NK cell function

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