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Pesquisa : D12.776.543.750.705.895.500.374 [Categoria DeCS]
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[PMID]:28202613
[Au] Autor:Thiruchelvam-Kyle L; Hoelsbrekken SE; Saether PC; Bjørnsen EG; Pende D; Fossum S; Daws MR; Dissen E
[Ad] Endereço:Division of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, 0317 Oslo, Norway; and lavanya.thiruchelvam-kyle@medisin.uio.no.
[Ti] Título:The Activating Human NK Cell Receptor KIR2DS2 Recognizes a ß -Microglobulin-Independent Ligand on Cancer Cells.
[So] Source:J Immunol;198(7):2556-2567, 2017 Apr 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The functions of activating members of the killer cell Ig-like receptor (KIR) family are not fully understood, as the ligands for these receptors are largely unidentified. In this study, we report that KIR2DS2 reporter cells recognize a ligand expressed by cancer cell lines. All cancer targets recognized by KIR2DS2 were also recognized by KIR2DL2 and KIR2DL3 reporters. Trogocytosis of membrane proteins from the cancer targets was observed with responding reporter cells, indicating the formation of KIR2DS2 ligand-specific immunological synapses. HLA-C typing of target cells showed that KIR2DS2 recognition was independent of the HLA C1 or C2 group, whereas targets cells that were only recognized by KIR2DL3 expressed C1 group alleles. Anti-HLA class I Abs blocked KIR2DL3 responses toward C1-expressing targets, but they did not block KIR2DS2 recognition of cancer cells. Small interfering RNA knockdown of ß -microglobulin reduced the expression of class I H chain on the cancer targets by >97%, but it did not reduce the KIR2DS2 reporter responses, indicating a ß -microglobulin-independent ligand for KIR2DS2. Importantly, KIR2DL3 responses toward some KIR2DS2 ligand-expressing cells were also undiminished after ß -microglobulin knockdown, and they were not blocked by anti-HLA class I Abs, suggesting that KIR2DL3, in addition to the traditional HLA-C ligands, can bind to the same ß -microglobulin-independent ligand as KIR2DS2. These observations indicate the existence of a novel, presently uncharacterized ligand for the activating NK cell receptor KIR2DS2. Molecular identification of this ligand may lead to improved KIR-HLA mismatching in hematopoietic stem cell transplantation therapy for leukemia and new, more specific NK cell-based cancer therapies.
[Mh] Termos MeSH primário: Neoplasias/metabolismo
Receptores KIR2DL2/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Separação Celular
Citometria de Fluxo
Técnicas de Silenciamento de Genes
Seres Humanos
Ligantes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, KIR2DL2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600930


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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]:27251940
[Au] Autor:Velarde-de la Cruz EE; Sánchez-Hernández PE; Muñoz-Valle JF; Palafox-Sánchez CA; Ramírez-de Los Santos S; Graciano-Machuca O; García-Iglesias T; Montoya-Buelna M; Ramírez-Dueñas MG
[Ad] Endereço:a Laboratorio de Inmunología, Departamento de Fisiología , Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara , Guadalajara , Jalisco , México ;
[Ti] Título:KIR2DL2 and KIR2DS2 as genetic markers to the methotrexate response in rheumatoid arthritis patients.
[So] Source:Immunopharmacol Immunotoxicol;38(4):303-9, 2016 Aug.
[Is] ISSN:1532-2513
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Disease Modifying Anti-Rheumatic Drugs (DMARDs) are aimed to interfere with rheumatoid arthritis (RA) progression and reduce the joint damage; however, not all patients respond alike. Killer-cell immunoglobulin-like receptors (KIR) and their ligands, human leucocyte antigen class I (HLA-I), have been associated with RA pathology; therefore, KIR and HLA genes may influence the treatment response. MATERIALS AND METHODS: We evaluated the association of KIR genotype and their ligands HLA-C genes with the response to DMARDs in RA patients. We included 69 patients diagnosed with RA and 82 healthy individuals as the reference group. KIR and HLA-C genotyping was performed using SSP-PCR. RA patients were assessed at baseline and under treatment at 6 and 12 months; subsequently classified as responders and non-responders in each time period. We evaluated the association between DMARD response and genes using statistical analysis by using Fisher exact test with Bonferroni correction; results were regarded as statistically significant at p < 0.05. RESULTS: Significant difference was observed in gene frequencies of patients and the reference group, KIR2DL2 was associated with RA (p = 0.031, OR = 2.119). We also observed an association between KIR2DS2 and the response to methotrexate (MTX), moreover, the combination KIR2DL2+/KIR2DS2+ was more frequent in responders to MTX (p = 0.043). DISCUSSION AND CONCLUSIONS: In our results, responders and non-responders to DMARDs showed KIR2DS2 and KIR2DL2 different gene frequencies, therefore, these genes could be used as response predictors to DMARDs treatment. Thus, these genes were also associated with disease severity, as well as the treatment response possibly by the immunoregulatory function of NK cells.
[Mh] Termos MeSH primário: Artrite Reumatoide/tratamento farmacológico
Artrite Reumatoide/genética
Genótipo
Metotrexato/administração & dosagem
Receptores KIR2DL2/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Adulto
Artrite Reumatoide/imunologia
Feminino
Marcadores Genéticos
Seres Humanos
Masculino
Meia-Idade
Receptores KIR/imunologia
Receptores KIR2DL2/imunologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Genetic Markers); 0 (KIR2DL2 protein, human); 0 (KIR2DS2 protein, human); 0 (Receptors, KIR); 0 (Receptors, KIR2DL2); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170321
[Lr] Data última revisão:
170321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE
[do] DOI:10.1080/08923973.2016.1194429


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[PMID]:27138091
[Au] Autor:Rizzo R; Bortolotti D; Fainardi E; Gentili V; Bolzani S; Baldi E; Casetta I; Granieri E; Rotola A; Furlan R; Di Luca D
[Ad] Endereço:Department of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, Italy. Electronic address: rbr@unife.it.
[Ti] Título:KIR2DL2 inhibitory pathway enhances Th17 cytokine secretion by NK cells in response to herpesvirus infection in multiple sclerosis patients.
[So] Source:J Neuroimmunol;294:1-5, 2016 05 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We have previously demonstrated that multiple sclerosis (MS) patients with KIR2DL2 expression on Natural killer (NK) cells are more susceptible to herpes simplex virus 1 (HSV-1) infection. We explored cytokine expression by NK cells during HSV-1 infection in association with KIR2DL2 expression. MS KIR2DL2(+) NK cells failed to control HSV-1 infection and secreted high levels of Th17 cytokines, while MS KIR2DL2(-) NK cells released Th1 cytokines, mainly IFN-gamma. Our data showed, for the first time, a peculiar Th17 cytokine secretion by MS KIR2DL2(+) NK cells in the presence of HSV-1 infection, that could be implicated in MS pathogenesis.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Herpes Simples
Células Matadoras Naturais/metabolismo
Esclerose Múltipla Recidivante-Remitente/patologia
Receptores KIR2DL2/metabolismo
[Mh] Termos MeSH secundário: Adulto
Células Cultivadas
Feminino
Seres Humanos
Células Matadoras Naturais/virologia
Ativação Linfocitária
Masculino
Meia-Idade
Esclerose Múltipla Recidivante-Remitente/virologia
RNA Mensageiro/metabolismo
Receptores KIR2DL2/genética
Células Th17/metabolismo
Carga Viral/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (KIR2DL2 protein, human); 0 (RNA, Messenger); 0 (Receptors, KIR2DL2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160504
[St] Status:MEDLINE


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[PMID]:27037558
[Au] Autor:Battistella M; Janin A; Jean-Louis F; Collomb C; Leboeuf C; Sicard H; Bonnafous C; Dujardin A; Ram-Wolff C; Kadin ME; Bensussan A; Bagot M; Michel L
[Ad] Endereço:Département de Pathologie, AP-HP, Hôpital Saint-Louis, Paris, 75010, France.
[Ti] Título:KIR3DL2 (CD158k) is a potential therapeutic target in primary cutaneous anaplastic large-cell lymphoma.
[So] Source:Br J Dermatol;175(2):325-33, 2016 Aug.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: KIR3DL2, an inhibitory receptor expressed by natural killer cells and a subset of normal CD8(+) T cells, is aberrantly expressed in neoplastic cells in transformed mycosis fungoides and Sézary syndrome. Anti-KIR3DL2 targeted antibody therapy has shown potent activity in preclinical models for these diseases. OBJECTIVES: To examine the expression of KIR3DL2 and its potential use as a therapeutic target in patients with primary cutaneous anaplastic large-cell lymphoma (pcALCL), the most aggressive cutaneous CD30(+) lymphoproliferative disease. METHODS: Samples from 11 patients with pcALCL and three CD30(+) lymphoproliferative disease cell lines - Mac1, Mac2a and Mac2b - were used in KIR3DL2 expression studies using immunohistochemistry, flow cytometry and reverse-transcriptase quantitative polymerase chain reaction. The effect of IPH4102, a monoclonal humanized IgG1 targeting KIR3DL2, was assessed by in vitro cytotoxicity assays against Mac1, Mac2a and Mac2b using allogeneic peripheral blood mononuclear cells as effectors. RESULTS: KIR3DL2 mRNA and protein were found in all human samples of pcALCL, and in the Mac2a and Mac2b cell lines. KIR3DL2 protein expression was present on 85·8 ± 14·0% of CD30(+) skin-infiltrating tumour cells. In vitro functional studies showed that KIR3DL2(+) Mac2a and Mac2b pcALCL lines are sensitive to antibody-derived cytotoxicity mediated by IPH4102, through activation of natural killer cells, in a concentration-dependent manner. CONCLUSIONS: pcALCL tumour cells express KIR3DL2, and we provide preclinical proof of concept for the use of IPH4102, a humanized anti-KIR3DL2 antibody, to treat patients with primary cutaneous CD30(+) ALCL.
[Mh] Termos MeSH primário: Linfoma Anaplásico de Células Grandes/tratamento farmacológico
Receptores KIR2DL2/antagonistas & inibidores
Neoplasias Cutâneas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Feminino
Seres Humanos
Antígeno Ki-1/metabolismo
Células Matadoras Naturais/fisiologia
Leucócitos Mononucleares/metabolismo
Masculino
Meia-Idade
Receptores KIR2DL2/imunologia
Receptores KIR2DL2/metabolismo
Pele/metabolismo
Células Tumorais Cultivadas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (KIR2DL2 protein, human); 0 (Ki-1 Antigen); 0 (Receptors, KIR2DL2)
[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:160403
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14626


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[PMID]:27030405
[Au] Autor:Bari R; Thapa R; Bao J; Li Y; Zheng J; Leung W
[Ad] Endereço:Department of Bone Marrow Transplantation and Cellular Therapy, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
[Ti] Título:KIR2DL2/2DL3-E(35) alleles are functionally stronger than -Q(35) alleles.
[So] Source:Sci Rep;6:23689, 2016 Mar 31.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:KIR2DL2 and KIR2DL3 segregate as alleles of a single locus in the centromeric motif of the killer cell immunoglobulin-like receptor (KIR) gene family. Although KIR2DL2/L3 polymorphism is known to be associated with many human diseases and is an important factor for donor selection in allogeneic hematopoietic stem cell transplantation, the molecular determinant of functional diversity among various alleles is unclear. In this study we found that KIR2DL2/L3 with glutamic acid at position 35 (E(35)) are functionally stronger than those with glutamine at the same position (Q(35)). Cytotoxicity assay showed that NK cells from HLA-C1 positive donors with KIR2DL2/L3-E(35) could kill more target cells lacking their ligands than NK cells with the weaker -Q(35) alleles, indicating better licensing of KIR2DL2/L3(+) NK cells with the stronger alleles. Molecular modeling analysis reveals that the glutamic acid, which is negatively charged, interacts with positively charged histidine located at position 55, thereby stabilizing KIR2DL2/L3 dimer and reducing entropy loss when KIR2DL2/3 binds to HLA-C ligand. The results of this study will be important for future studies of KIR2DL2/L3-associated diseases as well as for donor selection in allogeneic stem cell transplantation.
[Mh] Termos MeSH primário: Ácido Glutâmico/genética
Glutamina/genética
Antígenos HLA-C/genética
Células Matadoras Naturais/imunologia
Polimorfismo de Nucleotídeo Único
Receptores KIR2DL2/genética
Receptores KIR2DL3/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Linhagem Celular
Citotoxicidade Imunológica
Regulação da Expressão Gênica
Genótipo
Ácido Glutâmico/química
Ácido Glutâmico/imunologia
Glutamina/química
Glutamina/imunologia
Antígenos HLA-C/química
Antígenos HLA-C/imunologia
Seres Humanos
Células Matadoras Naturais/citologia
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Modelos Moleculares
Cultura Primária de Células
Ligação Proteica
Domínios Proteicos
Estrutura Secundária de Proteína
Receptores KIR2DL2/química
Receptores KIR2DL2/imunologia
Receptores KIR2DL3/química
Receptores KIR2DL3/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (KIR2DL2 protein, human); 0 (KIR2DL3 protein, human); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3); 0RH81L854J (Glutamine); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170130
[Lr] Data última revisão:
170130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160401
[St] Status:MEDLINE
[do] DOI:10.1038/srep23689


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[PMID]:26960450
[Au] Autor:Tozkir JD; Tozkir H; Gürkan H; Dönmez S; Eker D; Pamuk GE; Pamuk ÖN
[Ad] Endereço:Health Services Vocational College, Trakya University, Edirne, Turkey. jduymaz@gmail.com.
[Ti] Título:The investigation of killer cell immunoglobulin-like receptor genotyping in patients with systemic lupus erytematosus and systemic sclerosis.
[So] Source:Clin Rheumatol;35(4):919-25, 2016 Apr.
[Is] ISSN:1434-9949
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by the production of autoantibodies and the involvement of multiple organ systems. Systemic sclerosis (SSc) is another autoimmune disease that causes fibrosis. We will aim to analyse the role of killer cell immunoglobulin-like receptor (KIR) genotypes and their existence with the respective HLA ligands in patients with SLE and SSc. Forty-five SLE, 25 SSc and 40 healthy controls were included. We examined the presence/absence of KIR2DL1, 2DL2, 2DL3, 2DL4, 2DL5A, 2DL5B, 2DS1, 2DS1, 2DS2, 2DS3, 2DS4, 2DS5, 3DL1, 3DL2, 3DL3, 3DS1, 2DP1, 3DP1 and their known HLA ligands. In the SLE group, the KIR2DL5, KIR2DL5B and KIR2DS3 genes were significantly more frequent, and KIR2DL3 gene was significantly less than in controls (p values <0.05). In SSc patients, the KIR2DS3 gene was more frequent than in controls (p = 0.032). The KIR2DL3 gene was detected more frequently in controls while KIR2DS3 gene was more frequent in the patient group when SLE and SSc patients were combined (p values < 0.05). The KIR2DS2/HLA-C and KIR2DS2/HLA-C combinations were significantly more in both SLE and SSc groups than in controls. The KIR2DL2 and KIR2DL5B genes were protective from neurologic involvement in SLE patients (p values <0.05). The variations of some KIR genes such as KIR2DL5, KIR2DL5B, KIR2DS3 and KIR2DL3 may have a role in the pathogenesis of SLE and SSc. Also, the presence of KIR2DL2 and KIR2DL5B may cause major organ involvement, like neurologic involvement, in SLE.
[Mh] Termos MeSH primário: Genótipo
Lúpus Eritematoso Sistêmico/genética
Receptores KIR/genética
Escleroderma Sistêmico/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Estudos de Casos e Controles
Feminino
Frequência do Gene
Antígenos HLA-C/genética
Haplótipos
Seres Humanos
Ligantes
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Receptores KIR2DL2/genética
Receptores KIR2DL3/genética
Receptores KIR2DL5/genética
Escleroderma Sistêmico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (KIR2DL2 protein, human); 0 (KIR2DL3 protein, human); 0 (KIR2DL5B protein, human); 0 (KIR2DS3 protein, human); 0 (Ligands); 0 (Receptors, KIR); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3); 0 (Receptors, KIR2DL5)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160311
[St] Status:MEDLINE
[do] DOI:10.1007/s10067-016-3222-0


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[PMID]:26542067
[Au] Autor:Díaz-Peña R; Vidal-Castiñeira JR; Moro-García MA; Alonso-Arias R; Castro-Santos P
[Ad] Endereço:Department of Immunology, Hospital Universitario Central de Asturias, Oviedo, Spain; Faculty of Health Sciences, Universidad Autónoma de Chile, Talca, Chile.
[Ti] Título:Significant association of the KIR2DL3/HLA-C1 genotype with susceptibility to Crohn's disease.
[So] Source:Hum Immunol;77(1):104-9, 2016 Jan.
[Is] ISSN:1879-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We aimed to analyze the possible association of KIR/HLA-C genotypes with the susceptibility to Crohn's disease (CD) in a Spanish population. A total of 125 patients with CD and 339 healthy controls were selected for this study. KIR and HLA-C typing were developed by sequence-specific oligonucleotide probing. We found that the centromeric A/A genotype and HLA-C1 combination was significantly increased in CD patients (P<10(-3)). The KIR2DL3/2DL3 genotype was significantly increased in CD patients (P<0.0005). Moreover, we also observed a highly significant increase of KIR2DL3-HLA-C1 homozygosis in CD patients (P<0.0005). Our results confirm the relevance of the KIR2DL2/KIR2DL3 genes and their interaction with HLA-C to CD. We show that the contribution of the KIR genes to CD susceptibility extends beyond the association with individual KIRs, with an imbalance between activating and inhibitory KIR genes seeming to influence the susceptibility to CD.
[Mh] Termos MeSH primário: Doença de Crohn/imunologia
Antígenos HLA-C/genética
Células Matadoras Naturais/imunologia
Receptores KIR2DL2/genética
Receptores KIR2DL3/genética
[Mh] Termos MeSH secundário: Doença de Crohn/genética
Frequência do Gene
Estudos de Associação Genética
Predisposição Genética para Doença
Genótipo
Seres Humanos
Desequilíbrio de Ligação
Polimorfismo Genético
Espanha
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (KIR2DL2 protein, human); 0 (KIR2DL3 protein, human); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151107
[St] Status:MEDLINE


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[PMID]:26031759
[Au] Autor:Sanjeevi S; Sun C; Kanungo A; Sanjeevi CB
[Ad] Endereço:Department of Medicine (Solna), Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Killer immunoglobulin receptor genes and their HLA-C ligand are associated with Type 1 diabetes in an Eastern Indian population.
[So] Source:Diabet Med;33(1):91-6, 2016 Jan.
[Is] ISSN:1464-5491
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Killer immunoglobulin-like receptors (KIRs) and their interaction with HLA class I ligands have been shown to be associated with Type 1 diabetes mellitus. The aim of our study was to investigate the influence of KIR genes and their HLA-C ligands for susceptibility to Type 1 diabetes in patients from Eastern India. METHODS: A total of 135 patients with Type 1 diabetes and 98 healthy subjects from Eastern India were typed for KIR genes and HLA-C ligands using PCR-based genotyping. The frequencies of these genes were compared between patients and controls. RESULTS: Comparison of KIR genes between Type 1 diabetes patients and healthy subjects revealed significantly different frequencies of KIRs 2DL2 and 2DS4. The presence of HLA-C1 was negatively associated with disease. The presence of both HLA-C1 and -C2 showed a negative association with Type 1 diabetes, whereas the absence of C1 and presence of C2 was positively associated with disease. Stratification analysis of HLA-C ligands and KIRs showed significant associations between Type 1 diabetes and 2DL2+/C1-, 2DL2-/C1+, 2DL3+/C1+, 2DL3+/C1- and 2DS2+/C1-. CONCLUSIONS: Our results suggest that the interaction of KIRs with HLA-C ligands are significant and certain combinations contribute to susceptibility to and protection against Type 1 diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/genética
Predisposição Genética para Doença
Antígenos HLA-C/sangue
Células T Matadoras Naturais/metabolismo
Polimorfismo Genético
Receptores KIR2DL2/genética
Receptores KIR2DL3/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Alelos
Diabetes Mellitus Tipo 1/sangue
Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/metabolismo
Suscetibilidade a Doenças
Regulação da Expressão Gênica
Frequência do Gene
Estudos de Associação Genética
Antígenos HLA-C/genética
Antígenos HLA-C/metabolismo
Seres Humanos
Índia
Ligantes
Células T Matadoras Naturais/imunologia
Receptores KIR/agonistas
Receptores KIR/sangue
Receptores KIR/metabolismo
Receptores KIR2DL2/agonistas
Receptores KIR2DL2/sangue
Receptores KIR2DL2/metabolismo
Receptores KIR2DL3/agonistas
Receptores KIR2DL3/sangue
Receptores KIR2DL3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (KIR2DL2 protein, human); 0 (KIR2DL3 protein, human); 0 (KIR2DS4 protein, human); 0 (Ligands); 0 (Receptors, KIR); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150603
[St] Status:MEDLINE
[do] DOI:10.1111/dme.12815


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[PMID]:26453750
[Au] Autor:Anton OM; Vielkind S; Peterson ME; Tagaya Y; Long EO
[Ad] Endereço:Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852; and.
[Ti] Título:NK Cell Proliferation Induced by IL-15 Transpresentation Is Negatively Regulated by Inhibitory Receptors.
[So] Source:J Immunol;195(10):4810-21, 2015 Nov 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-15 bound to the IL-15Rα-chain (IL-15Rα) is presented in trans to cells bearing the IL-2Rß-chain and common γ-chain. As IL-15 transpresentation occurs in the context of cell-to-cell contacts, it has the potential for regulation by and of other receptor-ligand interactions. In this study, human NK cells were tested for the sensitivity of IL-15 transpresentation to inhibitory receptors. Human cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A were transfected with IL-15Rα. Proliferation of primary NK cells in response to transpresented IL-15 was reduced by engagement of either KIR2DL1 or KIR2DL2/3 by cognate HLA-C ligands. Inhibitory KIR-HLA-C interactions did not reduce the proliferation induced by soluble IL-15. Therefore, transpresentation of IL-15 is subject to downregulation by MHC class I-specific inhibitory receptors. Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E. Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein. IL-15Rα was not excluded from, but was evenly distributed across, inhibitory synapses. These findings demonstrate a novel mechanism to attenuate IL-15-dependent NK cell proliferation and suggest that inhibitory NK cell receptors contribute to NK cell homeostasis.
[Mh] Termos MeSH primário: Proliferação Celular/fisiologia
Interleucina-15/imunologia
Células Matadoras Naturais/imunologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Receptores KIR2DL1/imunologia
[Mh] Termos MeSH secundário: Feminino
Antígenos HLA-C/imunologia
Seres Humanos
Subunidade beta de Receptor de Interleucina-2/imunologia
Células Matadoras Naturais/citologia
Masculino
Fosforilação/imunologia
Proteínas Proto-Oncogênicas c-akt/imunologia
Receptores de Interleucina-15/imunologia
Receptores KIR2DL2/imunologia
Receptores KIR2DL3/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (IL15 protein, human); 0 (IL15RA protein, human); 0 (IL2RB protein, human); 0 (Interleukin-15); 0 (Interleukin-2 Receptor beta Subunit); 0 (KIR2DL1 protein, human); 0 (KIR2DL2 protein, human); 0 (KIR2DL3 protein, human); 0 (KLRD1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Receptors, Interleukin-15); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR2DL2); 0 (Receptors, KIR2DL3); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161115
[Lr] Data última revisão:
161115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1500414



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