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[PMID]:29180808
[Au] Autor:Barkal AA; Weiskopf K; Kao KS; Gordon SR; Rosental B; Yiu YY; George BM; Markovic M; Ring NG; Tsai JM; McKenna KM; Ho PY; Cheng RZ; Chen JY; Barkal LJ; Ring AM; Weissman IL; Maute RL
[Ad] Endereço:Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
[Ti] Título:Engagement of MHC class I by the inhibitory receptor LILRB1 suppresses macrophages and is a target of cancer immunotherapy.
[So] Source:Nat Immunol;19(1):76-84, 2018 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exciting progress in the field of cancer immunotherapy has renewed the urgency of the need for basic studies of immunoregulation in both adaptive cell lineages and innate cell lineages. Here we found a central role for major histocompatibility complex (MHC) class I in controlling the phagocytic function of macrophages. Our results demonstrated that expression of the common MHC class I component ß -microglobulin (ß2M) by cancer cells directly protected them from phagocytosis. We further showed that this protection was mediated by the inhibitory receptor LILRB1, whose expression was upregulated on the surface of macrophages, including tumor-associated macrophages. Disruption of either MHC class I or LILRB1 potentiated phagocytosis of tumor cells both in vitro and in vivo, which defines the MHC class I-LILRB1 signaling axis as an important regulator of the effector function of innate immune cells, a potential biomarker for therapeutic response to agents directed against the signal-regulatory protein CD47 and a potential target of anti-cancer immunotherapy.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe I/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/imunologia
Macrófagos/imunologia
Neoplasias/imunologia
Fagocitose/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Antígenos de Histocompatibilidade Classe I/metabolismo
Seres Humanos
Imunoterapia/métodos
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/metabolismo
Macrófagos/metabolismo
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos SCID
Neoplasias/metabolismo
Neoplasias/terapia
Neoplasias Experimentais/imunologia
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I); 0 (Leukocyte Immunoglobulin-like Receptor B1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1038/s41590-017-0004-z


  2 / 217 MEDLINE  
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[PMID]:29262349
[Au] Autor:Fu B; Zhou Y; Ni X; Tong X; Xu X; Dong Z; Sun R; Tian Z; Wei H
[Ad] Endereço:Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Te
[Ti] Título:Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors.
[So] Source:Immunity;47(6):1100-1113.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy. However, the role of NK cells in fetal growth is unclear. Here, we have identified a CD49a Eomes subset of NK cells that secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin, in both humans and mice. The crosstalk between HLA-G and ILT2 served as a stimulus for GPF-secreting function of this NK cell subset. Decreases in this GPF-secreting NK cell subset impaired fetal development, resulting in fetal growth restriction. The transcription factor Nfil3, but not T-bet, affected the function and the number of this decidual NK cell subset. Adoptive transfer of induced CD49a Eomes NK cells reversed impaired fetal growth and rebuilt an appropriate local microenvironment. These findings reveal properties of NK cells in promoting fetal growth. In addition, this research proposes approaches for therapeutic administration of NK cells in order to reverse restricted nourishments within the uterine microenvironment during early pregnancy.
[Mh] Termos MeSH primário: Aborto Habitual/imunologia
Transferência Adotiva
Proteínas de Transporte/secreção
Citocinas/secreção
Desenvolvimento Fetal/imunologia
Retardo do Crescimento Fetal/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Células Matadoras Naturais/transplante
[Mh] Termos MeSH secundário: Aborto Habitual/genética
Aborto Habitual/patologia
Adulto
Animais
Antígenos CD/genética
Antígenos CD/imunologia
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/imunologia
Proteínas de Transporte/genética
Proteínas de Transporte/imunologia
Microambiente Celular
Citocinas/genética
Citocinas/imunologia
Decídua/imunologia
Decídua/patologia
Feminino
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/imunologia
Retardo do Crescimento Fetal/patologia
Feto
Regulação da Expressão Gênica no Desenvolvimento
Antígenos HLA-G/genética
Antígenos HLA-G/imunologia
Seres Humanos
Integrina alfa1/genética
Integrina alfa1/imunologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/imunologia
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Gravidez
Transdução de Sinais
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Carrier Proteins); 0 (Cytokines); 0 (EOMES protein, human); 0 (HLA-G Antigens); 0 (Integrin alpha1); 0 (Intercellular Signaling Peptides and Proteins); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (NFIL3 protein, human); 0 (OGN protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 134034-50-7 (pleiotrophin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  3 / 217 MEDLINE  
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[PMID]:28664612
[Au] Autor:Rothe K; Raulien N; Köhler G; Pierer M; Quandt D; Wagner U
[Ad] Endereço:University of Leipzig, Department of Internal Medicine, Division of Rheumatology, Leipzig, Germany.
[Ti] Título:Autoimmune arthritis induces paired immunoglobulin-like receptor B expression on CD4 T cells from SKG mice.
[So] Source:Eur J Immunol;47(9):1457-1467, 2017 Sep.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The chronic, destructive autoimmune arthritis in SKG mice, which closely resembles human rheumatoid arthritis, is the result of self-reactive T cells escaping thymic deletion. Since the inhibitory receptor LIR-1 is up-regulated on auto-reactive T cells in human rheumatoid arthritis, the role of its murine ortholog PIR-B was investigated. Peripheral CD4 T cells from SKG mice were found to frequently express PIR-B, and this population produces more frequently IL-17 upon in vitro stimulation compared to PIR-B cells. A much larger fraction of PIR-B T cells, however, was found to secret no IL-17, but IFN-γ. With regards to the clinical course of the disease, high frequencies of PIR-B CD4 T cells were found to be associated with a milder course of arthritis, suggesting that the net effect of PIR-B expression is suppression of autoreactive T cells. Our results indicate that overexpression of PIR-B on IL-17-producing SKG CD4 T cells might represent an effective counter-regulatory mechanism against the destructive potential of those cells. More importantly, a major population of PIR-B T cells in SKG mice appears to play an inhibitory role by way of their IFN-γ production, since high frequencies of those cells ameliorate the disease.
[Mh] Termos MeSH primário: Artrite Experimental/imunologia
Artrite Reumatoide/imunologia
Linfócitos T CD4-Positivos/imunologia
Interferon gama/metabolismo
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Células Cultivadas
Feminino
Seres Humanos
Interleucina-17/metabolismo
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos
RNA Interferente Pequeno/genética
Receptores Imunológicos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Interleukin-17); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Pirb protein, mouse); 0 (RNA, Small Interfering); 0 (Receptors, Immunologic); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646747


  4 / 217 MEDLINE  
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[PMID]:28638976
[Au] Autor:van der Touw W; Chen HM; Pan PY; Chen SH
[Ad] Endereço:Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, New York, NY, 10029, USA.
[Ti] Título:LILRB receptor-mediated regulation of myeloid cell maturation and function.
[So] Source:Cancer Immunol Immunother;66(8):1079-1087, 2017 Aug.
[Is] ISSN:1432-0851
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The leukocyte immunoglobulin-like receptor (LILR) family comprises a set of paired immunomodulatory receptors expressed among human myeloid and lymphocyte cell populations. While six members of LILR subfamily A (LILRA) associate with membrane adaptors to signal via immunoreceptor tyrosine-based activating motifs (ITAM), LILR subfamily B (LILRB) members signal via multiple cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIM). Ligand specificity of some LILR family members has been studied in detail, but new perspective into the immunoregulatory aspects of this receptor family in human myeloid cells has been limited. LILRB receptors and the murine ortholog, paired immunoglobulin-like receptor B (PIRB), have been shown to negatively regulate maturation pathways in myeloid cells including mast cells, neutrophils, dendritic cells, as well as B cells. Our laboratory further demonstrated in mouse models that PIRB regulated functional development of myeloid-derived suppressor cell and the formation of a tumor-permissive microenvironment. Based on observations from the literature and our own studies, our laboratory is focusing on how LILRs modulate immune homeostasis of human myeloid cells and how these pathways may be targeted in disease states. Integrity of this pathway in tumor microenvironments, for example, permits a myeloid phenotype that suppresses antitumor adaptive immunity. This review presents the evidence supporting a role of LILRs as myeloid cell regulators and ongoing efforts to understand the functional immunology surrounding this family.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Leucócitos/imunologia
Células Supressoras Mieloides/imunologia
Neoplasias/imunologia
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imunomodulação
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Camundongos
Receptores Imunológicos/genética
Transdução de Sinais/imunologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Pirb protein, mouse); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1007/s00262-017-2023-x


  5 / 217 MEDLINE  
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[PMID]:28636952
[Au] Autor:Dulberger CL; McMurtrey CP; Hölzemer A; Neu KE; Liu V; Steinbach AM; Garcia-Beltran WF; Sulak M; Jabri B; Lynch VJ; Altfeld M; Hildebrand WH; Adams EJ
[Ad] Endereço:Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL 60637, USA.
[Ti] Título:Human Leukocyte Antigen F Presents Peptides and Regulates Immunity through Interactions with NK Cell Receptors.
[So] Source:Immunity;46(6):1018-1029.e7, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evidence is mounting that the major histocompatibility complex (MHC) molecule HLA-F (human leukocyte antigen F) regulates the immune system in pregnancy, infection, and autoimmunity by signaling through NK cell receptors (NKRs). We present structural, biochemical, and evolutionary analyses demonstrating that HLA-F presents peptides of unconventional length dictated by a newly arisen mutation (R62W) that has produced an open-ended groove accommodating particularly long peptides. Compared to empty HLA-F open conformers (OCs), HLA-F tetramers bound with human-derived peptides differentially stained leukocytes, suggesting peptide-dependent engagement. Our in vitro studies confirm that NKRs differentiate between peptide-bound and peptide-free HLA-F. The complex structure of peptide-loaded ß m-HLA-F bound to the inhibitory LIR1 revealed similarities to high-affinity recognition of the viral MHC-I mimic UL18 and a docking strategy that relies on contacts with HLA-F as well as ß m, thus precluding binding to HLA-F OCs. These findings provide a biochemical framework to understand how HLA-F could regulate immunity via interactions with NKRs.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe I/metabolismo
Células Matadoras Naturais/imunologia
Mimetismo Molecular
Receptores de Células Matadoras Naturais/metabolismo
Proteínas Virais/química
[Mh] Termos MeSH secundário: Apresentação do Antígeno
Antígenos/imunologia
Antígenos/metabolismo
Antígenos CD/metabolismo
Evolução Biológica
Cristalografia por Raios X
Feminino
Células HEK293
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Mutação/genética
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/metabolismo
Gravidez
Ligação Proteica
Conformação Proteica
Receptores Imunológicos/metabolismo
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Antigens, CD); 0 (HLA-F antigens); 0 (Histocompatibility Antigens Class I); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Peptide Fragments); 0 (Receptors, Immunologic); 0 (Receptors, Natural Killer Cell); 0 (Viral Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


  6 / 217 MEDLINE  
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[PMID]:28586095
[Au] Autor:Makwana N; Foley B; Fernandez S; Lee S; Irish A; Pircher H; Price P
[Ad] Endereço:Pathology & Laboratory Medicine, University of Western Australia, Nedlands, Australia.
[Ti] Título:CMV drives the expansion of highly functional memory T cells expressing NK-cell receptors in renal transplant recipients.
[So] Source:Eur J Immunol;47(8):1324-1334, 2017 Aug.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Cytomegalovirus (CMV) is a common opportunistic infection encountered in renal transplant recipients (RTRs) and may be reactivated without symptoms at any time post-transplant. We describe how active and latent CMV affect T-cell subsets in RTRs who are stable on maintenance therapy. T-cell responses to CMV were assessed in RTRs (n = 54) >2 years post-transplant, and healthy controls (n = 38). Seven RTRs had CMV DNA detectable in plasma. CMV antibody and DNA aligned with increased proportions of CD8 T cells and reduced CD4/CD8 ratios. This paralleled an expansion of effector memory T-cell (T ), terminally differentiated T-cell (T ) and CD57 T cell populations. Expression of NK-cell receptors, LIR-1 and KLRG1 on CD4 and CD8 CD57 T and T cells correlated with elevated interferon-γ and cytotoxic responses to anti-CD3 and increased cytotoxic responses to CMV phosphoprotein (pp) 65 in RTRs who carried CMV DNA. CD8 T cells from all CMV seropositive RTRs responded efficiently to CMV immediate early (IE) -1 peptides. The data show that latent and active CMV infection can alter T-cell subsets in RTRs many years after transplantation, and up-regulate T-cell expression of NK-cell receptors. This may enhance effector responses of CD4 and CD8 T cells against CMV.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Memória Imunológica
Transplante de Rim
Lectinas Tipo C/metabolismo
Receptores Imunológicos/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD/genética
Relação CD4-CD8
Antígenos CD57/genética
Antígenos CD57/imunologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Citomegalovirus/genética
Infecções por Citomegalovirus/virologia
DNA Viral/sangue
Feminino
Genes Precoces
Seres Humanos
Interferon gama/biossíntese
Interferon gama/imunologia
Células Matadoras Naturais/imunologia
Lectinas Tipo C/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Masculino
Meia-Idade
Peptídeos/farmacologia
Receptores Imunológicos/genética
Receptores de Células Matadoras Naturais/genética
Receptores de Células Matadoras Naturais/metabolismo
Transativadores/genética
Transplantados
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD57 Antigens); 0 (DNA, Viral); 0 (KLRG1 protein, human); 0 (LILRB1 protein, human); 0 (Lectins, C-Type); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Peptides); 0 (Receptors, Immunologic); 0 (Receptors, Natural Killer Cell); 0 (Trans-Activators); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747018


  7 / 217 MEDLINE  
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[PMID]:27562679
[Au] Autor:Makwana NB; Foley B; Lee S; Fernandez S; Irish AB; Price P
[Ad] Endereço:Pathology and Laboratory Medicine, University of Western Australia, Nedlands, Australia.
[Ti] Título:Asymptomatic CMV infections in long-term renal transplant recipients are associated with the loss of FcRγ from LIR-1 NK cells.
[So] Source:Eur J Immunol;46(11):2597-2608, 2016 Nov.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:While it is established that cytomegalovirus (CMV) disease affects NK-cell profiles, the functional consequences of asymptomatic CMV replication are unclear. Here, we characterize NK cells in clinically stable renal transplant recipients (RTRs; n = 48) >2 years after transplantation. RTRs and age-matched controls (n = 32) were stratified by their CMV serostatus and the presence of measurable CMV DNA. CMV antibody or CMV DNA influenced expression of NKG2C, LIR-1, NKp30, NKp46, and FcRγ, a signaling adaptor molecule, on CD56 NK cells. Phenotypic changes ascribed to CMV were clearer in RTRs than in control subjects and affected NK-cell function as assessed by TNF-α and CD107a expression. The most active NK cells were FcRγ LIR-1 NKG2C and displayed high antibody-dependent cell cytotoxicity responses in the presence of immobilized CMV glycoprotein B reactive antibody. However, perforin levels in supernatants from RTRs with active CMV replication were low. Overall we demonstrate that CMV can be reactivated in symptom-free renal transplant recipients, affecting the phenotypic, and functional profiles of NK cells. Continuous exposure to CMV may maintain and expand NK cells that lack FcRγ but express LIR-1.
[Mh] Termos MeSH primário: Antígenos CD/genética
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Células Matadoras Naturais/imunologia
Receptores de IgG/imunologia
Receptores Imunológicos/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Anticorpos Antivirais/sangue
Citotoxicidade Celular Dependente de Anticorpos
Antígenos CD/imunologia
Infecções Assintomáticas
Citomegalovirus/genética
Infecções por Citomegalovirus/virologia
Feminino
Seres Humanos
Transplante de Rim
Células Matadoras Naturais/metabolismo
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Masculino
Meia-Idade
Subfamília C de Receptores Semelhantes a Lectina de Células NK/genética
Receptor 1 Desencadeador da Citotoxicidade Natural/genética
Receptor 3 Desencadeador da Citotoxicidade Natural/genética
Perforina/análise
Fenótipo
Receptores de IgG/deficiência
Receptores de IgG/genética
Receptores Imunológicos/imunologia
Proteínas do Envelope Viral/imunologia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Antigens, CD); 0 (KLRC2 protein, human); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 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, Immunologic); 0 (Viral Envelope Proteins); 0 (glycoprotein B, Simplexvirus); 126465-35-8 (Perforin)
[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:160827
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646422


  8 / 217 MEDLINE  
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[PMID]:27320605
[Au] Autor:Eguchi H; Maeda A; Lo PC; Matsuura R; Esquivel EL; Asada M; Sakai R; Nakahata K; Yamamichi T; Umeda S; Deguchi K; Ueno T; Okuyama H; Miyagawa S
[Ad] Endereço:Department of Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. Electronic address: hiroshieguchi@hotmail.com.
[Ti] Título:HLA-G1, but Not HLA-G3, Suppresses Human Monocyte/Macrophage-mediated Swine Endothelial Cell Lysis.
[So] Source:Transplant Proc;48(4):1285-7, 2016 May.
[Is] ISSN:1873-2623
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The inhibitory function of HLA-G1, a class Ib molecule, on monocyte/macrophage-mediated cytotoxicity was examined. The expression of inhibitory receptors that interact with HLA-G, immunoglobulin-like transcript 2 (ILT2), ILT4, and KIR2DL4 (CD158d) on in vitro-generated macrophages obtained from peripheral blood mononuclear cells and the phorbol 12-myristate 13-acetate (PMA)-activated THP-1 cells were examined by flow cytometry. cDNAs of HLA-G1, HLA-G3, HLA-E, and human ß2-microglobulin were prepared, transfected into pig endothelial cells (PECs), and macrophage- and the THP-1 cell-mediated PEC cytolysis was then assessed. In vitro-generated macrophages expressed not only ILT2 and ILT4 but CD158d as well. The transgenic HLA-G1 on PEC indicated a significant suppression in macrophage-mediated cytotoxicity, which was equivalent to that of transgenic HLA-E. HLA-G1 was clearly expressed on the cell surface of PEC, whereas the levels of HLA-G3 were much lower and remained in the intracellular space. On the other hand, the PMA-activated THP-1 cell was less expressed these inhibitory molecules than in vitro-generated macrophages. Therefore, the HLA-G1 on PECs showed a significant but relatively smaller suppression to THP-1 cell-mediated cytotoxicity compared to in vitro-generated macrophages. These results indicate that by generating HLA-G1, but not HLA-G3, transgenic pigs can protect porcine grafts from monocyte/macrophage-mediated cytotoxicity.
[Mh] Termos MeSH primário: Antígenos HLA-G/fisiologia
Leucócitos Mononucleares/imunologia
Macrófagos/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Antígenos CD/metabolismo
Citocinas/metabolismo
Citotoxicidade Imunológica/fisiologia
Células Endoteliais/imunologia
Endotélio/imunologia
Citometria de Fluxo
Antígenos HLA-G/metabolismo
Seres Humanos
Células Matadoras Naturais/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Glicoproteínas de Membrana/metabolismo
Receptores Imunológicos/metabolismo
Receptores KIR2DL4/metabolismo
Suínos
Transfecção/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cytokines); 0 (HLA-G Antigens); 0 (KIR2DL4 protein, human); 0 (LILRB1 protein, human); 0 (LILRB2 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Membrane Glycoproteins); 0 (Receptors, Immunologic); 0 (Receptors, KIR2DL4)
[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:160621
[St] Status:MEDLINE


  9 / 217 MEDLINE  
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[PMID]:27129285
[Au] Autor:Khanolkar RC; Kalogeropoulos M; Lawrie A; Roghanian A; Vickers MA; Young NT
[Ad] Endereço:Division of Applied Medicine, Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom; rahul47@live.com.
[Ti] Título:Leukocyte Ig-Like receptor B1 restrains dendritic cell function through increased expression of the NF-κB regulator ABIN1/TNIP1.
[So] Source:J Leukoc Biol;100(4):737-746, 2016 Oct.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inhibitory receptors of the human leukocyte immunoglobulin-like receptor family are constitutively expressed on all myeloid cell types and regulate their functional activity. We demonstrate that ligation of the human leukocyte antigen class I-specific receptor LILRB1, during the differentiation of monocytes to dendritic cells in vitro, results in increased expression of the nuclear factor κB inhibitor protein ABIN1 (also known as TNIP1). Similarly increased expression of ABIN1/TNIP1 was observed in the "immunosuppressive" monocyte populations of patients with non-Hodgkin lymphoma ex vivo. Reducing expression of ABIN1/TNIP1 using small interfering ribonucleic acid allows dendritic cells and immunosuppressive monocytes to respond to stimulation by allowing nuclear factor κB translocation to the nucleus (P < 0.001), increasing cell surface expression of antigen presentation and costimulatory molecules (P < 0.01), increasing phagocytic capacity (P < 0.001), secreting proinflammatory cytokines (P < 0.01), and an increasing ability to stimulate T cell responses (P < 0.05). Our study, therefore, identifies an important functional role for ABIN1/TNIP1 in mediating the effects of LILRB1 ligation-induced inhibitory effects on immune responses. Our findings suggest that inhibiting the LILRB1-ABIN1/TNIP1 pathway in antigen-presenting cells could be a therapeutic approach to stimulate antitumor immune responses. Conversely, stimulation of the pathway may also ameliorate autoimmune diseases in which TNIP1 is a susceptibility gene.
[Mh] Termos MeSH primário: Antígenos CD/fisiologia
Proteínas de Ligação a DNA/biossíntese
Células Dendríticas/citologia
Monócitos/citologia
Mielopoese/fisiologia
NF-kappa B/metabolismo
Receptores Imunológicos/fisiologia
[Mh] Termos MeSH secundário: Apresentação do Antígeno
Núcleo Celular/metabolismo
Células Cultivadas
Citocinas/secreção
Proteínas de Ligação a DNA/genética
Células Dendríticas/imunologia
Regulação da Expressão Gênica/imunologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
Seres Humanos
Interleucina-4/farmacologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Linfoma não Hodgkin/sangue
Monócitos/efeitos dos fármacos
Monócitos/metabolismo
Fagocitose
Transporte Proteico
Interferência de RNA
RNA Interferente Pequeno/genética
Proteínas Recombinantes/farmacologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Receptors, Immunologic); 0 (Recombinant Proteins); 0 (TNIP1 protein, human); 207137-56-2 (Interleukin-4); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160430
[St] Status:MEDLINE


  10 / 217 MEDLINE  
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[PMID]:27109306
[Au] Autor:Baía D; Pou J; Jones D; Mandelboim O; Trowsdale J; Muntasell A; López-Botet M
[Ad] Endereço:Immunology Unit, University Pompeu Fabra, Barcelona, Spain.
[Ti] Título:Interaction of the LILRB1 inhibitory receptor with HLA class Ia dimers.
[So] Source:Eur J Immunol;46(7):1681-90, 2016 Jul.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Leukocyte immunoglobulin-like receptor subfamily B member 1 (LILRB1) has been reported to interact with a wide spectrum of HLA class I (HLA-I) molecules, albeit with different affinities determined by allelic polymorphisms and conformational features. HLA-G dimerization and the presence of intracellular Cys residues in HLA-B7 have been shown to be critical for their recognition by LILRB1. We hypothesized that dimerization of classical HLA class Ia molecules, previously detected in exosomes, might enhance their interaction with LILRB1. A soluble LILRB1-Fc fusion protein and a sensitive cellular reporter system expressing a LILRB1-ζ chimera were employed to assess receptor interaction with different HLA class Ia molecules transfected in the human lymphoblastoid 721.221 cell line. Under these conditions, intracellular Cys residues and HLA-I dimerization appeared associated with increased LILRB1 recognition. On the other hand, a marginal interaction of LILRB1 with primary monocytic cells, irrespective of their high HLA-I expression, was enhanced by type I interferon (IFN). This effect appeared disproportionate to the cytokine-induced increase of surface HLA-I expression and was accompanied by detection of HLA class Ia dimers. Altogether, the results support that a regulated assembly of these noncanonical HLA-I conformers during the immune response may enhance the avidity of their interaction with LILRB1.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Antígenos HLA-A/metabolismo
Multimerização Proteica
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Alelos
Sequência de Aminoácidos
Linhagem Celular
Expressão Gênica
Antígenos HLA-A/química
Antígenos HLA-A/genética
Antígenos HLA-A/imunologia
Antígeno HLA-B7/química
Antígeno HLA-B7/genética
Antígeno HLA-B7/imunologia
Antígeno HLA-B7/metabolismo
Seres Humanos
Interferon Tipo I/metabolismo
Interferon Tipo I/farmacologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/metabolismo
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Monócitos/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (HLA-A Antigens); 0 (HLA-B7 Antigen); 0 (Interferon Type I); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201546149



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