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[PMID]:28695287
[Au] Autor:Colucci F
[Ad] Endereço:Department of Obstetrics and Gynaecology, NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, University of Cambridge School of Clinical Medicine, Box 111, Hills Road, Cambridge, CB2 0SP, UK. fc287@medschl.cam.ac.uk.
[Ti] Título:The role of KIR and HLA interactions in pregnancy complications.
[So] Source:Immunogenetics;69(8-9):557-565, 2017 Aug.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Combinations of KIR and HLA genes associate with pregnancy complications as well as with many other clinical scenarios. Understanding how certain KIR and HLA genes influence the biology of a disease is, however, a formidable challenge. These are the two most variable gene families in the human genome. Moreover, the biology of a disease is best understood by studying the cells of the affected tissue. Natural Killer (NK) cells express KIR and are the most abundant leukocytes in the uterus. Most of our knowledge of NK cells is based on what we have learned from cells isolated from blood, but these are different from their tissue resident counterparts, including uterine NK (uNK) cells. Reproductive immunology faces an additional challenge: Two genotypes must be considered because both maternal and foetal HLA class I molecules may influence the outcome of pregnancy, most likely through interactions with maternal KIR expressed on uNK cells. Maternal uNK cells are not spontaneously cytotoxic and instead engage in interactions with trophoblast. We hypothesise that these interactions regulate allocation of resources between the foetus and the mother and may go wrong in diseases of pregnancy.
[Mh] Termos MeSH primário: Antígenos HLA/genética
Complicações na Gravidez/etiologia
Receptores KIR/genética
[Mh] Termos MeSH secundário: Aborto Habitual/etiologia
Feminino
Seres Humanos
Células Matadoras Naturais/imunologia
Gravidez
Complicações na Gravidez/genética
Complicações na Gravidez/imunologia
Receptores KIR2DL3/fisiologia
Útero/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA Antigens); 0 (KIR2DL3 protein, human); 0 (Receptors, KIR); 0 (Receptors, KIR2DL3)
[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/s00251-017-1003-9


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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]:28083606
[Au] Autor:Kandilarova SM; Paschen A; Mihaylova A; Ivanova M; Schadendorf D; Naumova E
[Ad] Endereço:Department of Clinical Immunology with Stem Cell Bank, Alexandrovska University Hospital, Medical University, 1431, Sofia, Bulgaria. sneji_jm@yahoo.com.
[Ti] Título:The Influence of HLA and KIR Genes on Malignant Melanoma Development and Progression.
[So] Source:Arch Immunol Ther Exp (Warsz);64(Suppl 1):73-81, 2016 Dec.
[Is] ISSN:1661-4917
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Many studies have described the role of killer immunoglobulin-like receptors (KIRs) and their cognate human leukocyte antigen (HLA) class I ligands in the immune protection against melanoma, but the effect of these markers on intra-individual variations in tumor development and progression has remained less clear. We performed KIR, HLA, and KIR/ligand analysis in 283 patients with malignant melanoma in order to evaluate their integrated influence on disease stage and progression. The patients were grouped according to AJCC staging, histological type of the primary tumor, progression, and survival rate. Analysis of HLA class I alleles revealed positive association of HLA-C*14 (Pc = 0.026, OR = 5.99) and negative association of HLA-C*02 (Pc = 0.026, OR = 0.43) with the disease. Decreased frequency of KIR2DS5 was observed in patients with rapid progression, as compared to those with slow progression. KIR BB genotype was prevalent in patients with metastasis (p = 0.004, OR = 0.025). KIR AA genotype was nearly twice as frequent in rapidly progressive cases, but without statistical relevance (p = 0.055, OR = 2.6). Significantly increased frequency of KIR2DL2 in the presence of C1 ligand (strong inhibition) was found in patients with AJCC III and IV, as compared to individuals with AJCC I stage (p = 0.045, OR = 1.93). In summary, our data imply that KIR/ligand gene content in patients could modulate the disease course towards unfavorable tumor behavior.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Antígenos HLA/genética
Melanoma/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Alelos
Motivos de Aminoácidos
Progressão da Doença
Feminino
Predisposição Genética para Doença
Genótipo
Antígeno HLA-A3/genética
Antígenos HLA-C/genética
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Células Matadoras Naturais/citologia
Ligantes
Masculino
Melanoma/imunologia
Meia-Idade
Polimorfismo Genético
Receptores KIR2DL3/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA Antigens); 0 (HLA-A3 Antigen); 0 (HLA-C Antigens); 0 (Histocompatibility Antigens Class I); 0 (Ligands); 0 (Receptors, KIR); 0 (Receptors, KIR2DL3)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170413
[Lr] Data última revisão:
170413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1007/s00005-016-0437-3


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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]:27506421
[Au] Autor:Lisovsky I; Isitman G; Tremblay-McLean A; Song R; DaFonseca S; Lebouche B; Routy JP; Bruneau J; Bernard NF
[Ad] Endereço:Research Institute of the McGill University Health Centre (MUHC), Montreal, Quebec, Canada.
[Ti] Título:The differential impact of natural killer (NK) cell education via KIR2DL3 and KIR3DL1 on CCL4 secretion in the context of in-vitro HIV infection.
[So] Source:Clin Exp Immunol;186(3):336-346, 2016 Dec.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Carriage of certain inhibitory natural killer (NK) cell receptor (iNKR)/HLA ligand pairs is associated with protection from infection and slow time to AIDS implicating NK cells in HIV control. NK cells acquire functional potential through education, which requires the engagement of iNKRs by their human leucocyte antigen (HLA) ligands. HIV infection down-regulates cell surface HLA-A/B, but not HLA-C/E. We investigated how NK cell populations expressing combinations of the iNKRs NKG2A, KIR2DL3 (2DL3) and KIR3DL1 (3DL1) responded to autologous HIV infected CD4 (iCD4) cells. Purified NK cells from HIV-uninfected individuals were stimulated with autologous HIV iCD4 or uninfected CD4 T cells. Using flow cytometry we gated on each of the 8 NKG2A 2DL3 3DL1 populations and analysed all possible combinations of interferon (IFN)-γ, CCL4 and CD107a functional subsets responding to iCD4 cells. Infected CD4 cells induced differential frequencies of NKG2A 2DL3 3DL1 populations with total IFN-γ , CCL4 and CD107a functional profiles. 2DL3 NKG2A NK cells had a higher frequency of responses to iCD4 than other populations studied. A higher frequency of 2DL3 NK cells responded to iCD4 from individuals that were not HLA-C1 homozygotes. These results show that 2DL3 NK cells are mediators of HIV-specific responses. Furthermore, responses of NK cell populations to iCD4 are influenced not only by NK cell education through specific KIR/HLA pairs, but also by differential HIV-mediated changes in HLA expression.
[Mh] Termos MeSH primário: Quimiocina CCL4/secreção
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/metabolismo
Receptores KIR2DL3/metabolismo
Receptores KIR3DL1/metabolismo
[Mh] Termos MeSH secundário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD4-Positivos/virologia
Células Cultivadas
Genótipo
Infecções por HIV/genética
Infecções por HIV/imunologia
Infecções por HIV/metabolismo
HIV-1/imunologia
Antígenos HLA/genética
Antígenos HLA/imunologia
Antígenos HLA-C/genética
Antígenos HLA-C/imunologia
Homozigoto
Seres Humanos
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/metabolismo
Ativação Linfocitária
Receptores KIR2DL3/genética
Receptores KIR3DL1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL4); 0 (HLA Antigens); 0 (HLA-C Antigens); 0 (KIR2DL3 protein, human); 0 (KIR3DL1 protein, human); 0 (Receptors, KIR2DL3); 0 (Receptors, KIR3DL1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160811
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12849


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[PMID]:27461217
[Au] Autor:Singh P; Dass JF
[Ad] Endereço:Bioinformatics Division, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, 632014, India.
[Ti] Título:A multifaceted computational report on the variants effect on KIR2DL3 and IFNL3 candidate gene in HCV clearance.
[So] Source:Mol Biol Rep;43(10):1101-17, 2016 Oct.
[Is] ISSN:1573-4978
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:HCV infection causes acute and chronic liver diseases including, cirrhosis and hepatocellular carcinoma. Following HCV infection, spontaneous clearance occurs in approximately 20 % of the population dependant upon HCV genotype. In this study, functional and non-functional variant analysis was executed for the classical and the latest HCV clearance candidate genes namely, KIR2DL3 and IFNL3. Initially, the functional effects of non-synonymous SNPs were assigned on exposing to homology based tools, SIFT, PolyPhen-2 and PROVEAN. Further, UTR and splice sites variants were scanned for the gene expression and regulation changes. Subsequently, the haplotype and CNV were also identified. The mutation H77Y of KIR2DL3 and R157Q, H156Y, S63L, R157W, F179V, H128R, T101M, R180C, and F176I of IFNL3 results in conservation, RMSD, total energy, stability, and secondary structures revealed a negative impact on the structural fitness. UTRscan and the splice site result indicate functional change, which may affect gene regulation and expression. The graphical display of selected population shows alleles like rs270779, rs2296370, rs10423751, rs12982559, rs9797797, and rs35987710 of KIR2DL3 and rs12972991, rs12980275, rs4803217, rs8109886, and rs8099917 of IFNL3 are in high LD with a measure of [Formula: see text] broadcasting its protective effect in HCV clearance. Similarly, CNV report suggests major DNA fragment loss that could have a profound impact on the gene expression affecting the overall phenotype. This roundup report specifies the effect of NK cell receptor, KIR2DL3 and IFNL3 variants that can have a better prospect in GWAS and immunogenetic studies leading to better understanding of HCV clearance and progression.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
Interleucinas/genética
Polimorfismo de Nucleotídeo Único
Receptores KIR2DL3/genética
[Mh] Termos MeSH secundário: Variações do Número de Cópias de DNA
Ligação Genética
Predisposição Genética para Doença
Genótipo
Hepatite C/genética
Hepatite C/virologia
Seres Humanos
Interleucinas/química
Receptores KIR2DL3/química
Remissão Espontânea
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL28B protein, human); 0 (Interleukins); 0 (KIR2DL3 protein, human); 0 (Receptors, KIR2DL3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE
[do] DOI:10.1007/s11033-016-4044-5


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[PMID]:27312286
[Au] Autor:Shao JY; Yin WW; Zhang QF; Liu Q; Peng ML; Hu HD; Hu P; Ren H; Zhang DZ
[Ad] Endereço:Department of Infectious Diseases, Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
[Ti] Título:Siglec-7 Defines a Highly Functional Natural Killer Cell Subset and Inhibits Cell-Mediated Activities.
[So] Source:Scand J Immunol;84(3):182-90, 2016 Sep.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sialic acid-binding immunoglobulin-like lectin-7 (Siglec-7) is an inhibitory receptor expressed on natural killer (NK) cells. In this study, we investigated the relationship between Siglec-7 expression and NK cell functions. Siglec-7 was highly expressed on NK cells and was preferentially expressed by mature NK cells from peripheral blood of healthy adults. Siglec-7(+) NK cells displayed higher levels of activating receptors CD38, CD16, DNAM1, NKp30 and NKp46, but lower levels of inhibitory receptors such as NKG2A and CD158b, compared with Siglec-7(-) NK cells. Functional tests showed that Siglec-7(+) NK cells displayed more CD107a degranulation and IFN-γ production than Siglec-7(-) NK cells. Siglec-7 inhibited NK cell functions when interacting with specific antibodies. These data suggest that Siglec-7 defines a highly functional NK cell subset and suppresses NK cell-mediated functions when cross-linked with specific antibodies.
[Mh] Termos MeSH primário: Antígenos de Diferenciação Mielomonocítica/imunologia
Imunidade Celular
Células Matadoras Naturais/imunologia
Lectinas/imunologia
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/genética
ADP-Ribosil Ciclase 1/imunologia
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação de Linfócitos T/genética
Antígenos de Diferenciação de Linfócitos T/imunologia
Degranulação Celular
Linhagem da Célula
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/imunologia
Regulação da Expressão Gênica
Seres Humanos
Imunofenotipagem
Interferon gama/genética
Interferon gama/imunologia
Células Matadoras Naturais/citologia
Lectinas/genética
Proteína 1 de Membrana Associada ao Lisossomo/genética
Proteína 1 de Membrana Associada ao Lisossomo/imunologia
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/imunologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília C de Receptores Semelhantes a Lectina de Células NK/imunologia
Receptor 1 Desencadeador da Citotoxicidade Natural/genética
Receptor 1 Desencadeador da Citotoxicidade Natural/imunologia
Receptor 3 Desencadeador da Citotoxicidade Natural/genética
Receptor 3 Desencadeador da Citotoxicidade Natural/imunologia
Receptores de IgG/genética
Receptores de IgG/imunologia
Receptores KIR2DL3/genética
Receptores KIR2DL3/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, Myelomonocytic); 0 (Antigens, Differentiation, T-Lymphocyte); 0 (CD226 antigen); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (IFNG protein, human); 0 (KLRC1 protein, human); 0 (Lectins); 0 (Lysosomal-Associated Membrane Protein 1); 0 (Membrane Glycoproteins); 0 (NCR1 protein, human); 0 (NCR3 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (Natural Cytotoxicity Triggering Receptor 1); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (Receptors, IgG); 0 (Receptors, KIR2DL3); 0 (SIGLEC7 protein, human); 82115-62-6 (Interferon-gamma); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160618
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12455


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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]:26744892
[Au] Autor:Littera R; Chessa L; Onali S; Figorilli F; Lai S; Secci L; La Nasa G; Caocci G; Arras M; Melis M; Cappellini S; Balestrieri C; Serra G; Conti M; Zolfino T; Casale M; Casu S; Pasetto MC; Barca L; Salustro C; Matta L; Scioscia R; Zamboni F; Faa G; Orrù S; Carcassi C
[Ad] Endereço:Regional Transplant Center, R. Binaghi Hospital, ASL 8, Cagliari, Italy.
[Ti] Título:Exploring the Role of Killer Cell Immunoglobulin-Like Receptors and Their HLA Class I Ligands in Autoimmune Hepatitis.
[So] Source:PLoS One;11(1):e0146086, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Natural killer cells are involved in the complex mechanisms underlying autoimmune diseases but few studies have investigated their role in autoimmune hepatitis. Killer immunoglobulin-like receptors are key regulators of natural killer cell-mediated immune responses. METHODS AND FINDINGS: KIR gene frequencies, KIR haplotypes, KIR ligands and combinations of KIRs and their HLA Class I ligands were investigated in 114 patients diagnosed with type 1 autoimmune hepatitis and compared with a group of 221 healthy controls. HLA Class I and Class II antigen frequencies were compared to those of 551 healthy unrelated families representative of the Sardinian population. In our cohort, type 1 autoimmune hepatitis was strongly associated with the HLA-B18, Cw5, DR3 haplotype. The KIR2DS1 activating KIR gene and the high affinity HLA-C2 ligands were significantly higher in patients compared to controls. Patients also had a reduced frequency of HLA-Bw4 ligands for KIR3DL1 and HLA-C1 ligands for KIR2DL3. Age at onset was significantly associated with the KIR2DS1 activating gene but not with HLA-C1 or HLA-C2 ligand groups. CONCLUSIONS: The activating KIR gene KIR2DS1 resulted to have an important predictive potential for early onset of type 1 autoimmune hepatitis. Additionally, the low frequency of the KIR-ligand combinations KIR3DL1/HLA-Bw4 and KIR2DL3/HLA-C1 coupled to the high frequency of the HLA-C2 high affinity ligands for KIR2DS1 could contribute to unwanted NK cell autoreactivity in AIH-1.
[Mh] Termos MeSH primário: Expressão Gênica/imunologia
Hepatite Autoimune/diagnóstico
Hepatite Autoimune/imunologia
Células Matadoras Naturais/imunologia
Fígado/imunologia
Receptores KIR/imunologia
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Feminino
Antígenos HLA-B/genética
Antígenos HLA-B/imunologia
Antígeno HLA-B18/genética
Antígeno HLA-B18/imunologia
Antígenos HLA-C/genética
Antígenos HLA-C/imunologia
Antígeno HLA-DR3/genética
Antígeno HLA-DR3/imunologia
Haplótipos
Hepatite Autoimune/genética
Hepatite Autoimune/patologia
Seres Humanos
Células Matadoras Naturais/patologia
Fígado/patologia
Masculino
Meia-Idade
Pacientes Ambulatoriais
Receptores KIR/genética
Receptores KIR2DL3/genética
Receptores KIR2DL3/imunologia
Receptores KIR3DL1/genética
Receptores KIR3DL1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (HLA-B Antigens); 0 (HLA-B18 Antigen); 0 (HLA-Bw4 antigen); 0 (HLA-C Antigens); 0 (HLA-C*05 antigen); 0 (HLA-DR3 Antigen); 0 (KIR2DL3 protein, human); 0 (KIR2DS1 protein, human); 0 (KIR3DL1 protein, human); 0 (Receptors, KIR); 0 (Receptors, KIR2DL3); 0 (Receptors, KIR3DL1)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0146086



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