Killer‐cell immunoglobulin‐like receptor (KIR) nomenclature report, 2002

Marsh, S. G. E.; Parham, Peter; Dupont, Bo; Geraghty, Dan; Trowsdale, John; Middleton, Derek; Vilches, Carlos; Carrington, Mary; Witt, Campbell S.; Guethlein, LA; Shilling, Heather; García, Celsa; Hsu, Katharine C.; Wain, Hester

doi:10.1046/j.1365-2370.2003.00383.x

Cited by 161 publications

(206 citation statements)

References 34 publications

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“…In general, KIR haplotypes divide simply into two functionally distinctive groups, namely, A and B. 22,23 Group A has a fixed number of genes that encode inhibitory receptors, with the exception of 2DS4, whereas group B, which are mostly activating KIR genes, exhibit much more variability in the number of KIR genes. These KIR haplotypes also affect the clinical outcomes of HSCT, but the impacts are variedly or sometimes inconsistently reported.…”

Section: Introductionmentioning

confidence: 99%

The beneficial impact of missing KIR ligands and absence of donor KIR2DS3 gene on outcome following unrelated hematopoietic SCT for myeloid leukemia in the Chinese population

Zhao

Lai

et al. 2010

Bone Marrow Transplant

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The effect of natural killer (NK) cell alloreactivity on the outcome of unrelated hematopoietic SCT (HSCT) remains a topic of debate. NK cell alloreactivity after allogeneic HSCT is regulated by killer-cell Ig-like receptors (KIRs). To investigate the influence of KIRs on outcome after unrelated HSCT, we retrospectively analyzed the HLA and KIR genotypes of 116 donorrecipient pairs. We found that missing KIR ligands in recipients were significantly associated with a decreased leukemic relapse risk (P ¼ 0.019, HR ¼ 0.329), mainly in myeloid disease (P ¼ 0.003, HR ¼ 0.193). This beneficial effect was seen in AML/myelodysplastic syndrome and also in chronic myeloid leukemia. In myeloid disease, missing KIR ligands also improved 5-year OS (P ¼ 0.034, HR ¼ 0.430) and disease-free survival (DFS) (P ¼ 0.024, HR ¼ 0.445). Meanwhile, the presence of donor-activating KIR2DS3 gene was associated with increased relapse risk (P ¼ 0.003, HR ¼ 5.046), decreased OS (P ¼ 0.004, HR ¼ 3.181) and DFS (P ¼ 0.003, HR ¼ 2.919) in myeloid disease. No effect was seen in patients with lymphoid disease. Our study indicated that, in unrelated HSCT for myeloid leukemia, missing KIR ligands in recipients offered a lower relapse risk and a long-term survival advantage. The presence of KIR2DS3 in the donor was an important risk factor for myeloid leukemia.

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Section: Introductionmentioning

confidence: 99%

The beneficial impact of missing KIR ligands and absence of donor KIR2DS3 gene on outcome following unrelated hematopoietic SCT for myeloid leukemia in the Chinese population

Zhao

Lai

et al. 2010

Bone Marrow Transplant

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“…First, KIR genes have evolved rapidly by mutation and recombination to generate multiple alleles at every locus. 12,13 Second and even more conspicuous, the KIR-gene content of different genomes is variable. 1,2,14 Only the genes that mark the ends (KIR3DL3 and KIR3DL2) and the middle (KIR3DP1 and KIR2DL4) of the KIR complex are shared by the vast majority of individuals, and they define two variably arranged regions or intervals: one centromeric (the genes between KIR3DL3 and KIR3DP1) and one telomeric (between KIR2DL4 and KIR3DL2).…”

Section: Introductionmentioning

confidence: 99%

Duplication, mutation and recombination of the human orphan gene KIR2DS3 contribute to the diversity of KIR haplotypes

et al. 2008

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The KIR2DS3 gene is an activating homologue of the inhibitory killer-cell immunoglobulin-like receptors (KIR) that recognize HLA-C molecules, enabling NK cells to survey the normal function of endogenous antigen presentation. The genetics of KIR2DS3 is complicated by the existence of alleles with similar coding sequences that map to different regions of the KIR complex in chromosome 19, or whose location in this complex is unknown. Here, by studying the family segregation of the KIR alleles 2DS3*001, *002 and *003N, and the distribution of these in unrelated individuals, we demonstrate the existence of two paralogous KIR2DS3 genes that can be inherited separately or, as it happens frequently in Caucasoids due to linkage disequilibrium, together. Each KIR2DS3 gene is almost invariably associated in its 5 0 end to a different copy of KIR2DL5, a gene previously shown to be duplicated in humans. KIR2DL5 and KIR2DS3 thus form two highly homologous gene clusters situated in the centromeric and the telomeric intervals of KIR haplotypes. Recombination between those clusters is the likely origin of new haplotypes, characterized in this study, which harbour further duplications or deletions of multiple KIR genes. Our results help understand the genetics of KIR2DS3 and the diversity of human KIR genotypes.

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“…13 The variety of KIR haplotypes B all contain a mixture of functional activating and inhibiting KIRs. 11,14 In previous reports on hematopoietic stem cell transplantation, significant associations were found between KIR genes (the presence of specific KIRs, the number of KIRs, mismatching of inhibitory KIRs with their respective HLA ligands) and clinical key parameters, including chronic graft-versus-host disease, which can manifest in the lungs as bronchiolitis obliterans and cytomegalovirus (CMV) reactivation. [15][16][17] Recent data demonstrated that in patients with BOS, the number of peripheral blood NK cells is decreased but an increased number are present in transplanted lungs compared with stable patients.…”

mentioning

confidence: 99%

The Killer Immunoglobulin-Like Receptor (KIR) Group A Haplotype is Associated With Bronchiolitis Obliterans Syndrome After Lung Transplantation

Erp

Graaf

Paantjens

et al. 2008

The Journal of Heart and Lung Transplantation

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Background:The development of bronchiolitis obliterans syndrome (BOS) after lung transplantation is associated with viral infections. Natural killer (NK) cells are involved in the lysis of viral infected cells, and their activation is largely controlled by activating and inhibitory killer immunoglobulin-like receptors (KIRs). We hypothesized that KIR ligand incompatibility and recipients' individual KIRs could influence the development of BOS and the incidence of cytomegalovirus reactivation after lung transplantation. Methods:The KIR gene contents were determined in 48 patients who received a lung transplant, and human leukocyte antigen (HLA)-Cw and HLA-Bw4 typing was performed on their respective donors. Results:BOS developed in 7 patients and cytomegalovirus reactivation occurred in 16. BOS developed in 5 of 19 patients homozygous for KIR haplotype A compared with 2 of 27 patients with KIR haplotype AB and B (homozygous; p ϭ 0.03; log-rank test). In none of the patients with BOS was the activating KIR2DS5 gene detected, whereas it was present in 35% of patients without BOS (p ϭ 0.04; log-rank test). No correlation was found between KIR gene content and cytomegalovirus reactivation. Conclusion: Our results suggest that the lack of activating KIRs may play an important role in the development of BOS but not in the control of cytomegalovirus reactivation after lung transplantation.

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Killer‐cell immunoglobulin‐like receptor (KIR) nomenclature report, 2002

Cited by 161 publications

References 34 publications

The beneficial impact of missing KIR ligands and absence of donor KIR2DS3 gene on outcome following unrelated hematopoietic SCT for myeloid leukemia in the Chinese population

The beneficial impact of missing KIR ligands and absence of donor KIR2DS3 gene on outcome following unrelated hematopoietic SCT for myeloid leukemia in the Chinese population

Duplication, mutation and recombination of the human orphan gene KIR2DS3 contribute to the diversity of KIR haplotypes

The Killer Immunoglobulin-Like Receptor (KIR) Group A Haplotype is Associated With Bronchiolitis Obliterans Syndrome After Lung Transplantation

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