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[PMID]:28695291
[Au] Autor:Hilton HG; Parham P
[Ad] Endereço:Departments of Structural Biology and Microbiology & Immunology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA, 94305, USA.
[Ti] Título:Missing or altered self: human NK cell receptors that recognize HLA-C.
[So] Source:Immunogenetics;69(8-9):567-579, 2017 Aug.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are fast-acting and versatile lymphocytes that are critical effectors of innate immunity, adaptive immunity, and placental development. Controlling NK cell function are the interactions between killer-cell immunoglobulin-like receptors (KIRs) and their HLA-A, HLA-B and HLA-C ligands. Due to the extensive polymorphism of both KIR and HLA class I, these interactions are highly diversified and specific combinations correlate with protection or susceptibility to a range of infectious, autoimmune, and reproductive disorders. Evolutionary, genetic, and functional studies are consistent with the interactions between KIR and HLA-C being the dominant control mechanism of human NK cells. In addition to their recognition of the C1 and C2 epitopes, increasing evidence points to KIR having a previously unrecognized selectivity for the peptide presented by HLA-C. This selectivity appears to be a conserved feature of activating KIR and may partly explain the slow progress made in identifying their HLA class I ligands. The peptide selectivity of KIR allows NK cells to respond, not only to changes in the surface expression of HLA-C, but also to the more subtle changes in the HLA-C peptidome, such as occur during viral infection and malignant transformation. Here, we review recent advances in understanding of human-specific KIR evolution and how the inhibitory and activating HLA-C receptors allow NK cells to respond to healthy cells, diseased cells, and the semi-allogeneic cells of the fetus.
[Mh] Termos MeSH primário: Antígenos HLA-C/fisiologia
Receptores de Células Matadoras Naturais/fisiologia
[Mh] Termos MeSH secundário: Haplótipos
Seres Humanos
Receptores KIR/fisiologia
Receptores KIR2DL1/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (Receptors, KIR); 0 (Receptors, KIR2DL1); 0 (Receptors, Natural Killer Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1007/s00251-017-1001-y


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[PMID]:28686681
[Au] Autor:Littera R; Piredda G; Argiolas D; Lai S; Congeddu E; Ragatzu P; Melis M; Carta E; Michittu MB; Valentini D; Cappai L; Porcella R; Alba F; Serra M; Loi V; Maddi R; Orrù S; La Nasa G; Caocci G; Cusano R; Arras M; Frongia M; Pani A; Carcassi C
[Ad] Endereço:Regional Transplant Center, R. Binaghi Hospital, ASSL Cagliari, ATS Sardegna, Italy.
[Ti] Título:KIR and their HLA Class I ligands: Two more pieces towards completing the puzzle of chronic rejection and graft loss in kidney transplantation.
[So] Source:PLoS One;12(7):e0180831, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Kidney transplantation is a life-saving treatment for patients with end-stage renal disease. However, despite progress in surgical techniques and patient management, immunological rejection continues to have a negative impact on graft function and overall survival. Incompatibility between donors and recipients for human leukocyte antigens (HLA) of the major histocompatibility complex (MHC) generates a series of complex cellular and humoral immune response mechanisms that are largely responsible for rejection and loss of graft function. Within this context, a growing amount of evidence shows that alloreactive natural killer (NK) cells play a critical role in the immune response mechanisms elicited by the allograft. Killer immunoglobulin-like receptors (KIRs) are prominent mediators of NK cell alloreactivity. METHODS AND FINDINGS: A cohort of 174 first cadaveric kidney allograft recipients and their donors were selected from a total cohort of 657 transplanted patients for retrospective immunogenetic analyses. Patients with HLA Class II mismatches were excluded. HLA Class I allele frequencies were compared among patients with chronic rejection, patients with stable graft function and a group of 2388 healthy controls. Activating and inhibitory KIR gene frequencies, KIR haplotypes, KIR-HLA ligand matches/mismatches and combinations of recipient KIRs and donor HLA Class I ligands were compared among patients with and without chronic rejection and a group of 221 healthy controls. Patients transplanted from donors homozygous for HLA-C1 antigens had a significantly higher risk for chronic rejection than patients transplanted from donors homozygous or heterozygous for HLA-C2 antigens or with epitopes belonging to the HLA-Bw4 ligand group. The Kaplan-Meier curves obtained by dividing the patients into 3 groups according to the presence or absence of one or both of the combinations of recipient KIRs and donor HLA ligands (rKIR2DL1/dHLA-C2 and rKIR3DL1/dHLA-Bw4) showed a significantly higher cumulative incidence of chronic rejection in the group of patients completely lacking these functional units. These patients showed a progressively stronger decline in modification of diet in renal disease-estimated glomerular filtration rate. CONCLUSIONS: KIR genotyping should be performed at the time of enrolment of patients on the waiting list for organ transplantation. In our study, a significantly higher risk of chronic rejection after kidney transplantation was observed when recipient (r) and donor (d) pairs completely lacked the two functional rKIR-dHLA ligand combinations rKIR2DL1/dHLA-C2 and rKIR3DL1/dHLA-Bw4. This immunogenetic profile corresponds to low levels of NK cell inhibition. Therefore, patients with this high risk profile could benefit from immunosuppressive therapy aimed at reducing NK-cell cytotoxicity.
[Mh] Termos MeSH primário: Rejeição de Enxerto/genética
Antígenos HLA-B/imunologia
Antígenos HLA-C/imunologia
Transplante de Rim
Receptores KIR2DL1/imunologia
Receptores KIR3DL1/imunologia
[Mh] Termos MeSH secundário: Adulto
Cadáver
Estudos de Casos e Controles
Feminino
Expressão Gênica
Taxa de Filtração Glomerular
Rejeição de Enxerto/imunologia
Rejeição de Enxerto/patologia
Sobrevivência de Enxerto/genética
Antígenos HLA-B/genética
Antígenos HLA-C/genética
Histocompatibilidade
Seres Humanos
Falência Renal Crônica/imunologia
Falência Renal Crônica/patologia
Falência Renal Crônica/cirurgia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/patologia
Ligantes
Masculino
Meia-Idade
Receptores KIR2DL1/genética
Receptores KIR3DL1/genética
Transplante Homólogo
Doadores não Relacionados
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-B Antigens); 0 (HLA-Bw4 antigen); 0 (HLA-C Antigens); 0 (KIR2DL1 protein, human); 0 (KIR3DL1 protein, human); 0 (Ligands); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR3DL1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180831


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[PMID]:28558022
[Au] Autor:Cimini E; Viola D; Cabeza-Cabrerizo M; Romanelli A; Tumino N; Sacchi A; Bordoni V; Casetti R; Turchi F; Martini F; Bore JA; Koundouno FR; Duraffour S; Michel J; Holm T; Zekeng EG; Cowley L; Garcia Dorival I; Doerrbecker J; Hetzelt N; Baum JHJ; Portmann J; Wölfel R; Gabriel M; Miranda O; Díaz G; Díaz JE; Fleites YA; Piñeiro CA; Castro CM; Koivogui L; Magassouba N; Diallo B; Ruibal P; Oestereich L; Wozniak DM; Lüdtke A; Becker-Ziaja B; Capobianchi MR; Ippolito G; Carroll MW; Günther S; Di Caro A; Muñoz-Fontela C; Agrati C
[Ad] Endereço:Department of Epidemiology and Pre-clinical research, National Institute for Infectious Diseases "Lazzaro Spallanzani", Rome, Italy.
[Ti] Título:Different features of Vδ2 T and NK cells in fatal and non-fatal human Ebola infections.
[So] Source:PLoS Negl Trop Dis;11(5):e0005645, 2017 May.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Human Ebola infection is characterized by a paralysis of the immune system. A signature of αß T cells in fatal Ebola infection has been recently proposed, while the involvement of innate immune cells in the protection/pathogenesis of Ebola infection is unknown. Aim of this study was to analyze γδ T and NK cells in patients from the Ebola outbreak of 2014-2015 occurred in West Africa, and to assess their association with the clinical outcome. METHODOLOGY/PRINCIPAL FINDINGS: Nineteen Ebola-infected patients were enrolled at the time of admission to the Ebola Treatment Centre in Guinea. Patients were divided in two groups on the basis of the clinical outcome. The analysis was performed by using multiparametric flow cytometry established by the European Mobile Laboratory in the field. A low frequency of Vδ2 T-cells was observed during Ebola infection, independently from the clinical outcome. Moreover, Vδ2 T-cells from Ebola patients massively expressed CD95 apoptotic marker, suggesting the involvement of apoptotic mechanisms in Vδ2 T-cell loss. Interestingly, Vδ2 T-cells from survivors expressed an effector phenotype and presented a lower expression of the CTLA-4 exhaustion marker than fatalities, suggesting a role of effector Vδ2 T-cells in the protection. Furthermore, patients with fatal Ebola infection were characterized by a lower NK cell frequency than patients with non fatal infection. In particular, both CD56bright and CD56dim NK frequency were very low both in fatal and non fatal infections, while a higher frequency of CD56neg NK cells was associated to non-fatal infections. Finally, NK activation and expression of NKp46 and CD158a were independent from clinical outcome. CONCLUSIONS/SIGNIFICANCES: Altogether, the data suggest that both effector Vδ2 T-cells and NK cells may play a role in the complex network of protective response to EBOV infection. Further studies are required to characterize the protective effector functions of Vδ2 and NK cells.
[Mh] Termos MeSH primário: Doença pelo Vírus Ebola/imunologia
Doença pelo Vírus Ebola/mortalidade
Células Matadoras Naturais/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Subpopulações de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Antígeno CD56/metabolismo
Antígeno CTLA-4/metabolismo
Bases de Dados Factuais
Ebolavirus
Feminino
Citometria de Fluxo
Guiné/epidemiologia
Seres Humanos
Ativação Linfocitária/imunologia
Masculino
Receptor 1 Desencadeador da Citotoxicidade Natural/metabolismo
Receptores KIR2DL1/metabolismo
Carga Viral
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD56 Antigen); 0 (CTLA-4 Antigen); 0 (FAS protein, human); 0 (NCR1 protein, human); 0 (Natural Cytotoxicity Triggering Receptor 1); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, KIR2DL1); 0 (fas Receptor)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005645


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[PMID]:28122963
[Au] Autor:Hilton HG; Blokhuis JH; Guethlein LA; Norman PJ; Parham P
[Ad] Endereço:Department of Structural Biology, School of Medicine, Stanford University, Stanford, CA 94305; and hhilton@stanford.edu peropa@stanford.edu.
[Ti] Título:Resurrecting KIR2DP1: A Key Intermediate in the Evolution of Human Inhibitory NK Cell Receptors That Recognize HLA-C.
[So] Source:J Immunol;198(5):1961-1973, 2017 Mar 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is an inactive member of the human family, which includes all HLA-C-specific receptor genes. The lethal, and only, defect in is a nucleotide deletion in codon 88. Fixed in modern humans, the deletion is also in archaic human genomes. is polymorphic, with dimorphism at specificity-determining position 44. By repairing the deletion, we resurrected 11 alleles of , the functional antecedent of We demonstrate how K44-KIR2DP1 with lysine 44 recognized C1 HLA-C, whereas T44-KIR2DP1 recognized C2 HLA-C. Dimorphisms at 12 other KIR2DP1 residues modulate receptor avidity or signaling. KIR2DP1 and KIR2DL1 are neighbors in the centromeric region and are in tight linkage disequilibrium. Like , contributed to and haplotype differences. Encoded on , C1-specific K44-KIR2DP1 were stronger receptors than the attenuated C2-specific T44-KIR2DP1 encoded on The last common ancestor of humans and chimpanzees had diverse that passed on to chimpanzees but not to humans. Early humans inherited activating and an inhibitory , likely encoding a C1-specific receptor. The latter spawned the modern family of HLA-C receptors. KIR2DP1 has properties consistent with having been the founder gene. The first alleles encoded K44-C1 receptors; subsequently alleles encoding T44-C2 receptors evolved. The emergence of dedicated and genes encoding C1 and C2 receptors, respectively, could have led to obsolescence of Alternatively, pathogen subversion caused its demise. Preservation of functional polymorphism was a side effect of fixation of the deletion in by micro gene conversion.
[Mh] Termos MeSH primário: Evolução Biológica
Antígenos HLA-C/genética
Antígenos HLA-C/imunologia
Receptores KIR/genética
Receptores KIR/imunologia
[Mh] Termos MeSH secundário: Alelos
Animais
Antígenos HLA-C/fisiologia
Haplótipos
Seres Humanos
Células Matadoras Naturais/imunologia
Desequilíbrio de Ligação
Pan troglodytes
Polimorfismo Genético
Receptores KIR2DL1/química
Receptores KIR2DL1/genética
Receptores KIR2DL1/imunologia
Receptores KIR2DL2/genética
Receptores KIR2DL2/imunologia
Receptores KIR2DL3/genética
Receptores KIR2DL3/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (Receptors, KIR); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601835


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[PMID]:27751789
[Au] Autor:Moffett A; Chazara O; Colucci F; Johnson MH
[Ad] Endereço:Dept of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK; Centre for Trophoblast Research, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. Electronic address: am485@cam.ac.uk.
[Ti] Título:Variation of maternal KIR and fetal HLA-C genes in reproductive failure: too early for clinical intervention.
[So] Source:Reprod Biomed Online;33(6):763-769, 2016 Dec.
[Is] ISSN:1472-6491
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A distinctive type of (uterine) natural killer (NK) cell is present in the uterine decidua during the period of placental formation. Uterine NK cells express members of the killer immunoglobulin-like receptor (KIR) family that bind to parental HLA-C molecules on the invading placental trophoblast cells. The maternal KIR genes and their fetal ligands are highly variable, so different KIR/HLA-C genetic combinations occur in each pregnancy. Some women only possess inhibitory KIR genes, whereas other women also express activating KIR genes. The overall signal that NK cells receive from paternal HLA-C on trophoblast depends on the ratio of activating and inhibitory KIR genes expressed by them. Therefore, NK cells provide a balance during placentation to ensure maternal survival and an adequately nourished fetus. Because inhibitory KIRs are found more frequently in women with defective placentation, e.g. pre-eclampsia, fetal growth restriction or recurrent spontaneous abortion, some fertility clinics suggest that women should be 'tissue typed' for their KIR genotypes. We explain why, presently, it is premature to introduce KIR and HLA-C typing to predict pregnancy outcome. In future, however, selecting for certain combinations of KIR and HLA-C variants in surrogacy, egg or sperm donation may prove useful to reduce disorders of pregnancy.
[Mh] Termos MeSH primário: Antígenos HLA-C/genética
Infertilidade/genética
Receptores KIR2DL1/genética
Útero/metabolismo
[Mh] Termos MeSH secundário: Aborto Habitual/etiologia
Estudos de Coortes
Decídua/metabolismo
Epitopos/química
Feminino
Genótipo
Antígenos HLA-C/metabolismo
Haplótipos
Homozigoto
Seres Humanos
Células Matadoras Naturais/metabolismo
Ligantes
Placenta/metabolismo
Placentação
Pré-Eclâmpsia/fisiopatologia
Gravidez
Receptores KIR2DL1/metabolismo
Recombinação Genética
Reprodução
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epitopes); 0 (HLA-C Antigens); 0 (KIR2DL1 protein, human); 0 (Ligands); 0 (Receptors, KIR2DL1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161019
[St] Status:MEDLINE


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[PMID]:27732638
[Au] Autor:Isitman G; Tremblay-McLean A; Lisovsky I; Bruneau J; Lebouché B; Routy JP; Bernard NF
[Ad] Endereço:Research Institute of the McGill University Health Centre (RI-MUHC), Montreal, Quebec, Canada.
[Ti] Título: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.
[So] Source:PLoS One;11(10):e0164517, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural Killer (NK) cell education, which requires the engagement of inhibitory NK cell receptors (iNKRs) by their ligands, is important for generating self-tolerant functional NK cells. While the potency of NK cell education is directly related to their functional potential upon stimulation with HLA null cells, the influence of NK cell education on the potency of the antibody dependent cellular cytotoxicity (ADCC) function of NK cells is unclear. ADCC occurs when the Fc portion of an immunoglobulin G antibody bridges the CD16 Fc receptor on NK cells and antigen on target cells, resulting in NK cell activation, cytotoxic granule release, and target cell lysis. We previously reported that education via the KIR3DL1/HLA-Bw4 iNKR/HLA ligand combination supported higher KIR3DL1+ than KIR3DL1- NK cell activation levels but had no impact on ADCC potency measured as the frequency of granzyme B positive (%GrB+) targets generated in an ADCC GranToxiLux assay. A lower frequency of KIR3DL1+ compared to KIR3DL1- NK cells were CD16+, which may in part explain the discrepancy between NK cell activation and target cell effects. Here, we investigated the frequency of CD16+ cells among NK cells expressing other iNKRs. We found that CD16+ cells were significantly more frequent among NK cells negative for the inhibitory KIR (iKIR) KIR2DL1, KIR2DL3, and KIR3DL1 than those positive for any one of these iKIR to the exclusion of the others, making iKIR+ NK cells poorer ADCC effectors than iKIR- NK cells. The education status of these iKIR+ populations had no effect on the frequency of CD16+ cells.
[Mh] Termos MeSH primário: Citotoxicidade Celular Dependente de Anticorpos
Células Matadoras Naturais/imunologia
Receptores de IgG/imunologia
Receptores KIR2DL1/imunologia
Receptores KIR2DL3/imunologia
Receptores KIR3DL1/imunologia
[Mh] Termos MeSH secundário: Células Cultivadas
Proteínas Ligadas por GPI/análise
Proteínas Ligadas por GPI/imunologia
Seres Humanos
Receptores de IgG/análise
Receptores KIR2DL1/análise
Receptores KIR2DL3/análise
Receptores KIR3DL1/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (KIR2DL1 protein, human); 0 (KIR2DL3 protein, human); 0 (KIR3DL1 protein, human); 0 (Receptors, IgG); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR2DL3); 0 (Receptors, KIR3DL1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164517


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[PMID]:27577226
[Au] Autor:Sun G; Wang C; Zhen J; Zhang G; Xu Y; Deng Z
[Ad] Endereço:Immunogenetics Laboratory, Shenzhen Blood Center, Shenzhen, Guangdong 518035, China; School of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning 116044, China. Email: zhihui_deng@aliyun.com.
[Ti] Título:[Cloning and sequencing of KIR2DL1 framework gene cDNA and identification of a novel allele].
[So] Source:Zhonghua Yi Xue Yi Chuan Xue Za Zhi;33(5):694-7, 2016 Oct.
[Is] ISSN:1003-9406
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To develop an assay for cDNA cloning and haplotype sequencing of KIR2DL1 framework gene and determine the genotype of an ethnic Han from southern China. METHODS: Total RNA was isolated from peripheral blood sample, and complementary DNA (cDNA) transcript was synthesized by RT-PCR. The entire coding sequence of the KIR2DL1 framework gene was amplified with a pair of KIR2DL1-specific PCR primers. The PCR products with a length of approximately 1.2 kb were then subjected to cloning and haplotype sequencing. RESULTS: A specific target fragment of the KIR2DL1 framework gene was obtained. Following allele separation, a wild-type KIR2DL1*00302 allele and a novel variant allele, KIR2DL1*031, were identified. Sequence alignment with KIR2DL1 alleles from the IPD-KIR Database showed that the novel allele KIR2DL1*031 has differed from the closest allele KIR2DL1*00302 by a non-synonymous mutation at CDS nt 188A>G (codon 42 GAG>GGG) in exon 4, which has caused an amino acid change Glu42Gly. The sequence of the novel allele KIR2DL1*031 was submitted to GenBank under the accession number KP025960 and to the IPD-KIR Database under the submission number IWS40001982. A name KIR2DL1*031 has been officially assigned by the World Health Organization (WHO) Nomenclature Committee. CONCLUSION: An assay for cDNA cloning and haplotype sequencing of KIR2DL1 has been established, which has a broad applications in KIR studies at allelic level.
[Mh] Termos MeSH primário: DNA Complementar/genética
Mutação de Sentido Incorreto
Receptores KIR2DL1/genética
Análise de Sequência de DNA/métodos
[Mh] Termos MeSH secundário: Alelos
Sequência de Bases
China
Clonagem Molecular
DNA Complementar/química
Haplótipos
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (KIR2DL1 protein, human); 0 (Receptors, KIR2DL1)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170105
[Lr] Data última revisão:
170105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1003-9406.2016.05.026


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[PMID]:27465324
[Au] Autor:Zou Y; Song ZX; Lu Y; Liang XL; Yuan Q; Liao SH; Bao JJ
[Ad] Endereço:Department of Blood Transfusion, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China.
[Ti] Título:Up-regulation of NKG2A inhibitory receptor on circulating NK cells contributes to transfusion-induced immunodepression in patients with ß-thalassemia major.
[So] Source:J Huazhong Univ Sci Technolog Med Sci;36(4):509-13, 2016 Aug.
[Is] ISSN:1672-0733
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence has shown that allogeneic blood transfusions can induce significant immunosuppression in recipients, and thereby increase the risk of postoperative infection and/or tumor relapse. Although it is well known that natural killer (NK) cells are responsible for the immunodepression effects of transfusion, the underlying mechanisms remain obscure. In this study, we investigated the role of NK cells in transfusion-induced immunodepression in ß-thalassemia major. The proportion of circulating NK cells and the expression of NK receptors (NKG2A, CD158a, NKP30, NKP46 and NKG2D) as well as CD107a were detected by multicolor flow cytometry. IFN-γ production by circulating NK cells was detected by intracellular cytokine staining. Our results showed that the proportion and cytotoxicity (CD107a expression) of circulating NK cells in transfusion-dependent ß-thalassemia major patients were remarkably lower than those of ß-thalassemia minor patients or healthy volunteers. Expression of NKG2A inhibitory receptor on circulating NK cells in patients with ß-thalassemia major was remarkably up-regulated, but there were no significant differences in the expression levels of NKP30, NKP46, NKG2D, CD158a and IFN-γ. These results indicate NKG2A inhibitory receptor may play a key role in transfusion-induced immunodepression of NK cells in patients with ß-thalassemia major.
[Mh] Termos MeSH primário: Células Matadoras Naturais/metabolismo
Subfamília C de Receptores Semelhantes a Lectina de Células NK/sangue
Talassemia beta/sangue
Talassemia beta/imunologia
[Mh] Termos MeSH secundário: Adolescente
Criança
Feminino
Citometria de Fluxo
Regulação da Expressão Gênica
Seres Humanos
Imunossupressão
Células Matadoras Naturais/imunologia
Masculino
Subfamília C de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/sangue
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Receptor 1 Desencadeador da Citotoxicidade Natural/sangue
Receptor 1 Desencadeador da Citotoxicidade Natural/imunologia
Receptor 3 Desencadeador da Citotoxicidade Natural/sangue
Receptor 3 Desencadeador da Citotoxicidade Natural/imunologia
Receptores KIR2DL1/sangue
Receptores KIR2DL1/imunologia
Reação Transfusional
Talassemia beta/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KLRK1 protein, human); 0 (NCR1 protein, human); 0 (NCR3 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Natural Cytotoxicity Triggering Receptor 1); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (Receptors, KIR2DL1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1007/s11596-016-1616-5


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[PMID]:27116381
[Au] Autor:Djaoud Z; Riou R; Gavlovsky PJ; Mehlal S; Bressollette C; Gérard N; Gagne K; Charreau B; Retière C
[Ad] Endereço:Etablissement Franx00E7;ais du Sang, ImmunoVirologie et Polymorphisme Gx00E9;nx00E9;tique, Universitx00E9; de Nantes, Nantes, France.
[Ti] Título:Cytomegalovirus-Infected Primary Endothelial Cells Trigger NKG2C+ Natural Killer Cells.
[So] Source:J Innate Immun;8(4):374-85, 2016.
[Is] ISSN:1662-8128
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Among innate cells, natural killer (NK) cells play a crucial role in the defense against cytomegalovirus (CMV). In some individuals, CMV infection induces the expansion of NKG2C+ NK cells that persist after control of the infection. We have previously shown that KIR2DL+ NK cells, in contrast to NKG2C+ NK cells, contribute to controlling CMV infection using a CMV-infected monocyte-derived dendritic cell (MDDC) model. However, the nature of CMV-infected cells contributing to the expansion of the NKG2C+ NK cell subset remains unclear. To gain more insight into this question, we investigated the contribution of NKG2C+ NK cell activation by CMV-infected primary human aortic endothelial cells (EC) isolated from kidney transplant donors, which constitutively express the human leukocyte antigen (HLA)-E molecule. Here, we show that, although classic HLA class I expression was drastically downregulated, nonclassic HLA-E expression was maintained in CMV-infected EC. By comparing HLA expression patterns in CMV-infected EC, fibroblasts and MDDC, we demonstrate a cell-dependent modulation of HLA-E expression by CMV infection. NKG2C+ NK cell degranulation was significantly triggered by CMV-infected EC regardless of the nature of the HLA-E allele product. EC, predominantly present in vessels, may constitute a privileged site for CMV infection that drives a 'memory' NKG2C+ NK cell subset.
[Mh] Termos MeSH primário: Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Células Dendríticas/imunologia
Endotélio Vascular/imunologia
Fibroblastos/imunologia
Células Matadoras Naturais/imunologia
Subpopulações de Linfócitos/imunologia
[Mh] Termos MeSH secundário: Aorta/patologia
Degranulação Celular
Proliferação Celular
Células Cultivadas
Células Dendríticas/virologia
Endotélio Vascular/virologia
Fibroblastos/virologia
Antígenos de Histocompatibilidade Classe I/genética
Antígenos de Histocompatibilidade Classe I/metabolismo
Seres Humanos
Memória Imunológica
Células Matadoras Naturais/virologia
Ativação Linfocitária
Subpopulações de Linfócitos/virologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptores KIR2DL1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-E antigen); 0 (Histocompatibility Antigens Class I); 0 (KIR2DL1 protein, human); 0 (KLRC2 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (Receptors, KIR2DL1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160427
[St] Status:MEDLINE
[do] DOI:10.1159/000445320


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[PMID]:26945896
[Au] Autor:Stelma F; Jansen L; Sinnige MJ; van Dort KA; Takkenberg RB; Janssen HL; Reesink HW; Kootstra NA
[Ad] Endereço:Department of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, the Netherlands.
[Ti] Título:HLA-C and KIR combined genotype as new response marker for HBeAg-positive chronic hepatitis B patients treated with interferon-based combination therapy.
[So] Source:J Viral Hepat;23(8):652-9, 2016 08.
[Is] ISSN:1365-2893
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Current treatment for chronic hepatitis B infection (CHB) consists of interferon-based therapy. However, for unknown reasons, a large proportion of patients with CHB do not respond to this treatment. Hence, there is a pressing need to establish response markers to select patients who will benefit from therapy and to spare potential nonresponders from unnecessary side effects of antiviral therapy. Here, we assessed whether HLA-C and KIR genotypes were associated with treatment outcome for CHB. Twelve SNPs in or near the HLA-C gene were genotyped in 86 CHB patients (41 HBeAg positive; 45 HBeAg negative) treated with peginterferon alfa-2a + adefovir. Genotyping of killer immunoglobin-like receptors (KIRs) was performed by SSP-PCR. One SNP in HLA-C (rs2308557) was significantly associated with combined response in HBeAg-positive CHB patients (P = 0.003). This SNP is linked to the HLA-C group C1 or C2 classification, which controls KIR binding. The combination of KIR2DL1 with its ligand HLA-C2 was observed significantly more often in HBeAg-positive patients with a combined response (13/14) than in nonresponders (11/27, P = 0.001). Patients with the KIR2DL1/C2 genotype had significantly higher baseline ALT levels (136 vs 50 U/L, P = 0.002) than patients without this combination. Furthermore, KIR2DL1-C2 predicted response independent of HBV genotype and ALT at baseline. HLA-C and KIR genotype is strongly associated with response in HBeAg-positive CHB patients treated with interferon-based therapy. In combination with other known response markers, HLA-C/KIR genotype could enable the selection of patients more likely to respond to interferon-based therapy.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Antígenos HLA-C/genética
Antígenos E da Hepatite B/sangue
Hepatite B Crônica/tratamento farmacológico
Hepatite B Crônica/genética
Interferons/uso terapêutico
Receptores KIR2DL1/genética
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/análise
Quimioterapia Combinada/métodos
Feminino
Hepatite B Crônica/diagnóstico
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Biomarkers); 0 (HLA-C Antigens); 0 (Hepatitis B e Antigens); 0 (KIR2DL1 protein, human); 0 (Receptors, KIR2DL1); 9008-11-1 (Interferons)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160307
[St] Status:MEDLINE
[do] DOI:10.1111/jvh.12525



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