Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.852.760.048 [Categoria DeCS]
Referências encontradas : 1585 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 159 ir para página                         

  1 / 1585 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28461108
[Au] Autor:Santaguida MG; Gatto I; Mangino G; Virili C; Stramazzo I; Fallahi P; Antonelli A; Segni M; Romeo G; Centanni M
[Ad] Endereço:Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome, Latina, Italy.
[Ti] Título:BREG cells in Hashimoto's thyroiditis isolated or associated to further organ-specific autoimmune diseases.
[So] Source:Clin Immunol;184:42-47, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hashimoto thyroiditis (HT) may occur isolated or associated with other non-endocrine autoimmune disorders (NEAD). No data are available about Breg cells in these disorders and this represented the aim of the study. Th17 and Breg cells subset were characterized on peripheral blood mononuclear cells isolated from 18 healthy donors (HD), 19 patients with isolated HT and 26 patients with HT+NEAD. Th17 were higher in patients with isolated HT than in HD but no further changes were seen in patients with HT+NEAD. CD24 CD38 unstimulated Breg cells were similar in HT patients and in HD, but significantly higher in patients with HT+NEAD than in both HT and in HD. CD19 CD24 CD27 Breg memory phenotype was similar in HD and in HT patients, but decreased in patients with HT+NEAD (23.4%vs38.5%). Upon CpG-stimulation, CD24 CD38 IL-10 Breg cells were higher in HT patients than in HD (3.9%vs1.8%) but similar in patients with HT+NEAD (2.4%).
[Mh] Termos MeSH primário: Linfócitos B Reguladores/imunologia
Doença Celíaca/imunologia
Gastrite Atrófica/imunologia
Doença de Hashimoto/imunologia
Células Th17/imunologia
Vitiligo/imunologia
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/imunologia
Adulto
Antígenos CD19/imunologia
Doenças Autoimunes/complicações
Doenças Autoimunes/imunologia
Antígeno CD24/imunologia
Estudos de Casos e Controles
Doença Celíaca/complicações
Feminino
Gastrite Atrófica/complicações
Doença de Hashimoto/complicações
Seres Humanos
Interleucina-10/imunologia
Masculino
Glicoproteínas de Membrana/imunologia
Meia-Idade
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
Vitiligo/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD19 molecule, human); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (IL10 protein, human); 0 (Membrane Glycoproteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 130068-27-8 (Interleukin-10); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  2 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29198913
[Au] Autor:Turaj AH; Hussain K; Cox KL; Rose-Zerilli MJJ; Testa J; Dahal LN; Chan HTC; James S; Field VL; Carter MJ; Kim HJ; West JJ; Thomas LJ; He LZ; Keler T; Johnson PWM; Al-Shamkhani A; Thirdborough SM; Beers SA; Cragg MS; Glennie MJ; Lim SH
[Ad] Endereço:Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK; Cancer Research UK Centre, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK.
[Ti] Título:Antibody Tumor Targeting Is Enhanced by CD27 Agonists through Myeloid Recruitment.
[So] Source:Cancer Cell;32(6):777-791.e6, 2017 Dec 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monoclonal antibodies (mAbs) can destroy tumors by recruiting effectors such as myeloid cells, or targeting immunomodulatory receptors to promote cytotoxic T cell responses. Here, we examined the therapeutic potential of combining a direct tumor-targeting mAb, anti-CD20, with an extended panel of immunomodulatory mAbs. Only the anti-CD27/CD20 combination provided cures. This was apparent in multiple lymphoma models, including huCD27 transgenic mice using the anti-huCD27, varlilumab. Detailed mechanistic analysis using single-cell RNA sequencing demonstrated that anti-CD27 stimulated CD8 T and natural killer cells to release myeloid chemo-attractants and interferon gamma, to elicit myeloid infiltration and macrophage activation. This study demonstrates the therapeutic advantage of using an immunomodulatory mAb to regulate lymphoid cells, which then recruit and activate myeloid cells for enhanced killing of mAb-opsonized tumors.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Antineoplásicos/farmacologia
Linfoma/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/agonistas
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Imunoterapia/métodos
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/imunologia
Ativação de Macrófagos/efeitos dos fármacos
Ativação de Macrófagos/imunologia
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (varlilumab)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  3 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28471362
[Au] Autor:Teplyakov A; Obmolova G; Malia TJ; Gilliland GL
[Ad] Endereço:Janssen Research and Development LLC, 1400 McKean Road, Spring House, PA 19477, USA.
[Ti] Título:Crystal structure of CD27 in complex with a neutralizing noncompeting antibody.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 5):294-299, 2017 May 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD27 is a T-cell and B-cell co-stimulatory glycoprotein of the tumor necrosis factor (TNF) receptor superfamily that is dependent on the availability of the TNF-like ligand CD70. Therapeutic approaches to treating autoimmune diseases and cancers with antagonistic and agonistic anti-CD27 monoclonal antibodies (mAbs), respectively, have recently been developed. Mouse anti-human CD27 mAb 2177 shows potency in neutralizing CD70-induced signaling; however, it does not block the binding of soluble CD70. To provide insight into the mechanism of action of the mAb, the crystal structure of the CD27 extracellular domain in complex with the Fab fragment of mAb 2177 was determined at 1.8 Šresolution. CD27 exhibits the assembly of cysteine-rich domains characteristic of the TNF receptor superfamily. The structure reveals a unique binding site of mAb 2177 at the edge of the receptor molecule, which allows the mAb to sterically block the cell-bound form of CD70 from reaching CD27 while leaving the ligand epitope clear. This mode of action suggests a potential dual use of mAb 2177 either as an antagonist or as an agonist.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/química
Anticorpos Neutralizantes/química
Complexo Antígeno-Anticorpo/química
Ligante CD27/química
Fragmentos Fab das Imunoglobulinas/química
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/química
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Animais
Anticorpos Monoclonais/genética
Anticorpos Neutralizantes/genética
Complexo Antígeno-Anticorpo/genética
Baculoviridae/genética
Baculoviridae/metabolismo
Sítios de Ligação
Ligante CD27/genética
Ligante CD27/imunologia
Clonagem Molecular
Cristalografia por Raios X
Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Células HEK293
Seres Humanos
Fragmentos Fab das Imunoglobulinas/genética
Ligantes
Camundongos
Modelos Moleculares
Ligação Proteica
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Alinhamento de Sequência
Células Sf9
Spodoptera
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Antigen-Antibody Complex); 0 (CD27 Ligand); 0 (CD70 protein, human); 0 (Immunoglobulin Fab Fragments); 0 (Ligands); 0 (Recombinant Fusion Proteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X17005957


  4 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27778417
[Au] Autor:Martins C; Lima J; Nunes G; Borrego LM
[Ad] Endereço:CEDOC, Chronic Diseases Research Center, Immunology, NOVA Medical School|FCM, Universidade Nova de Lisboa, Lisbon, Portugal.
[Ti] Título:Pregnancy alters the circulating B cell compartment in atopic asthmatic women, and transitional B cells are positively associated with the development of allergy manifestations in their progeny.
[So] Source:Am J Reprod Immunol;76(6):465-474, 2016 Dec.
[Is] ISSN:1600-0897
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:PROBLEM: Maternal atopy is a risk factor for allergy. B cells are poorly studied in reproduction and atopy. We aimed to assess how pregnancy affects B cells in atopic women and whether B cells relate to allergic manifestations in offspring. METHOD OF STUDY: Women with and without atopic asthma, pregnant and non-pregnant were enrolled for the study, and circulating B cells were evaluated by flow cytometry, using CD19, CD27, CD38, IgD, and IgM. RESULTS: Compared to healthy non-pregnant, atopic asthmatic non-pregnant (ANP) women presented increased B cell counts, enlarged memory subsets, less transitional cells, and plasmablasts. Atopic asthmatic pregnant (AP) and healthy pregnant (HP) women showed similarities: reduced B cell counts and percentages, fewer memory cells, especially switched, and higher plasmablast percentages. Transitional B cell percentages were increased in AP women with allergic manifestations in their progeny. CONCLUSION: Atopic asthmatic non-pregnant women have a distinctive B cell compartment. B cells change in pregnancy, similarly in AP and HP women. The recognition that AP women with allergy in their progeny have a typical immune profile may help, in the future, the adoption of preventive measures to avoid the manifestation of allergic diseases in their newborns.
[Mh] Termos MeSH primário: Asma/imunologia
Linfócitos B/imunologia
Hipersensibilidade Imediata/imunologia
Memória Imunológica
Herança Materna/imunologia
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/genética
ADP-Ribosil Ciclase 1/imunologia
Adulto
Antígenos CD19/genética
Antígenos CD19/imunologia
Asma/diagnóstico
Asma/genética
Asma/patologia
Linfócitos B/patologia
Estudos de Casos e Controles
Feminino
Expressão Gênica
Seres Humanos
Hipersensibilidade Imediata/diagnóstico
Hipersensibilidade Imediata/genética
Hipersensibilidade Imediata/patologia
Imunoglobulina D/sangue
Imunoglobulina M/sangue
Imunofenotipagem
Recém-Nascido
Doenças do Recém-Nascido
Contagem de Linfócitos
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/imunologia
Gravidez
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD19 molecule, human); 0 (Immunoglobulin D); 0 (Immunoglobulin M); 0 (Membrane Glycoproteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171130
[Lr] Data última revisão:
171130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/aji.12595


  5 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28886017
[Au] Autor:Moura RA; Quaresma C; Vieira AR; Gonçalves MJ; Polido-Pereira J; Romão VC; Martins N; Canhão H; Fonseca JE
[Ad] Endereço:Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
[Ti] Título:B-cell phenotype and IgD-CD27- memory B cells are affected by TNF-inhibitors and tocilizumab treatment in rheumatoid arthritis.
[So] Source:PLoS One;12(9):e0182927, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The use of TNF-inhibitors and/or the IL-6 receptor antagonist, tocilizumab, in rheumatoid arthritis (RA) have pleiotropic effects that also involve circulating B-cells. The main goal of this study was to assess the effect of TNF-inhibitors and tocilizumab on B-cell phenotype and gene expression in RA. METHODS: Blood samples were collected from untreated early RA (ERA) patients, established RA patients under methotrexate treatment, established RA patients before and after treatment with TNF-inhibitors and tocilizumab, and healthy donors. B-cell subpopulations were characterized by flow cytometry and B-cell gene expression was analyzed by real-time PCR on isolated B-cells. Serum levels of BAFF, CXCL13 and sCD23 were determined by ELISA. RESULTS: The frequency of total CD19+ B cells in circulation was similar between controls and all RA groups, irrespective of treatment, but double negative (DN) IgD-CD27- memory B cells were significantly increased in ERA and established RA when compared to controls. Treatment with TNF-inhibitors and tocilizumab restored the frequency of IgD-CD27- B-cells to normal levels, but did not affect other B cell subpopulations. TACI, CD95, CD5, HLA-DR and TLR9 expression on B-cells significantly increased after treatment with either TNF-inhibitors and/ or tocilizumab, but no significant changes were observed in BAFF-R, BCMA, CD69, CD86, CXCR5, CD23, CD38 and IgM expression on B-cells when comparing baseline with post-treatment follow-ups. Alterations in B-cell gene expression of BAFF-R, TACI, TLR9, FcγRIIB, BCL-2, BLIMP-1 and ß2M were found in ERA and established RA patients, but no significant differences were observed after TNF-inhibitors and tocilizumab treatment when comparing baseline and follow-ups. Serum levels of CXCL13, sCD23 and BAFF were not significantly affected by treatment with TNF-inhibitors and tocilizumab. CONCLUSIONS: In RA patients, the use of TNF-inhibitors and/ or tocilizumab treatment affects B-cell phenotype and IgD-CD27- memory B cells in circulation, but not B-cell gene expression levels.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Artrite Reumatoide/imunologia
Subpopulações de Linfócitos B/imunologia
Memória Imunológica
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/farmacologia
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Subpopulações de Linfócitos B/efeitos dos fármacos
Subpopulações de Linfócitos B/metabolismo
Biomarcadores
Quimiocina CXCL13/sangue
Seguimentos
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Imunoglobulina D/metabolismo
Imunofenotipagem
Contagem de Linfócitos
Metotrexato/farmacologia
Metotrexato/uso terapêutico
Fenótipo
Receptores CXCR5/metabolismo
Receptores de IgE/sangue
Resultado do Tratamento
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Biomarkers); 0 (Chemokine CXCL13); 0 (Immunoglobulin D); 0 (Receptors, CXCR5); 0 (Receptors, IgE); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (Tumor Necrosis Factor-alpha); I031V2H011 (tocilizumab); YL5FZ2Y5U1 (Methotrexate)
[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:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182927


  6 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28855314
[Au] Autor:Muschaweckh A; Petermann F; Korn T
[Ad] Endereço:Klinikum Rechts der Isar, Neurologische Klinik, Technische Universität München, 81675 Munich, Germany; and.
[Ti] Título:IL-1ß and IL-23 Promote Extrathymic Commitment of CD27 CD122 γδ T Cells to γδT17 Cells.
[So] Source:J Immunol;199(8):2668-2679, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:γδT17 cells are a subset of γδ T cells committed to IL-17 production and are characterized by the expression of IL-23R and CCR6 and lack of CD27 expression. γδT17 cells are believed to arise within a narrow time window during prenatal thymic development. In agreement with this concept, we show in this study that adult recipient mice of (IL-23R reporter) bone marrow selectively lack IL-23R γδT17 cells. Despite their absence in secondary lymphoid tissues during homeostasis, γδT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (Aldara). We demonstrate that IL-1ß and IL-23 together are able to promote the development of bona fide γδT17 cells from peripheral CD122 IL-23R γδ T cells, whereas CD122 γδ T cells fail to convert into γδT17 cells and remain stable IFN-γ producers (γδT1 cells). IL-23 is instrumental in expanding extrathymically generated γδT17 cells. In particular, TCR-Vγ4 chain-expressing CD122 IL-23R γδ T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation. In contrast, TCR-Vγ1 γδ T cells largely resist this process because prior TCR engagement in the thymus has initiated their commitment to the γδT1 lineage. In summary, our data reveal that the peripheral pool of γδ T cells retains a considerable degree of plasticity because it harbors "naive" precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually occupied by thymus-derived γδT17 cells.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Psoríase/imunologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Aminoquinolinas
Animais
Diferenciação Celular
Células Cultivadas
Modelos Animais de Doenças
Seres Humanos
Interleucina-1beta/metabolismo
Subunidade beta de Receptor de Interleucina-2/metabolismo
Interleucina-23/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Receptores de Interleucina/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (Interleukin-2 Receptor beta Subunit); 0 (Interleukin-23); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-23 receptor, mouse); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700287


  7 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28848067
[Au] Autor:Nakayama Y; Kosek J; Capone L; Hur EM; Schafer PH; Ringheim GE
[Ad] Endereço:Inflammation and Immunology Translational Development, Celgene Corporation, Summit, NJ 07901.
[Ti] Título:Aiolos Overexpression in Systemic Lupus Erythematosus B Cell Subtypes and BAFF-Induced Memory B Cell Differentiation Are Reduced by CC-220 Modulation of Cereblon Activity.
[So] Source:J Immunol;199(7):2388-2407, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BAFF is a B cell survival and maturation factor implicated in the pathogenesis of systemic lupus erythematosus (SLE). In this in vitro study, we describe that soluble BAFF in combination with IL-2 and IL-21 is a T cell contact-independent inducer of human B cell proliferation, plasmablast differentiation, and IgG secretion from circulating CD27 memory and memory-like CD27 IgD double-negative (DN) B cells, but not CD27 IgD naive B cells. In contrast, soluble CD40L in combination with IL-2 and IL-21 induces these activities in both memory and naive B cells. Blood from healthy donors and SLE patients have similar circulating levels of IL-2, whereas SLE patients exhibit elevated BAFF and DN B cells and reduced IL-21. B cell differentiation transcription factors in memory, DN, and naive B cells in SLE show elevated levels of Aiolos, whereas Ikaros levels are unchanged. Treatment with CC-220, a modulator of the cullin ring ligase 4-cereblon E3 ubiquitin ligase complex, reduces Aiolos and Ikaros protein levels and BAFF- and CD40L-induced proliferation, plasmablast differentiation, and IgG secretion. The observation that the soluble factors BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implications for extrafollicular plasmablast development within inflamed tissue. Inhibition of B cell plasmablast differentiation by reduction of Aiolos and Ikaros may have utility in the treatment of SLE, where elevated levels of BAFF and Aiolos may prime CD27 memory and DN memory-like B cells to become Ab-producing plasmablasts in the presence of BAFF and proinflammatory cytokines.
[Mh] Termos MeSH primário: Fator Ativador de Células B/sangue
Fator Ativador de Células B/imunologia
Subpopulações de Linfócitos B/imunologia
Fator de Transcrição Ikaros/genética
Memória Imunológica
Lúpus Eritematoso Sistêmico/imunologia
Peptídeo Hidrolases/metabolismo
[Mh] Termos MeSH secundário: Formação de Anticorpos/efeitos dos fármacos
Fator Ativador de Células B/metabolismo
Subpopulações de Linfócitos B/efeitos dos fármacos
Ligante de CD40/farmacologia
Diferenciação Celular
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Seres Humanos
Fator de Transcrição Ikaros/sangue
Memória Imunológica/efeitos dos fármacos
Interleucina-2/sangue
Interleucina-2/farmacologia
Interleucinas/farmacologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/deficiência
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (CC-220); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (IKZF1 protein, human); 0 (IKZF3 protein, human); 0 (Interleukin-2); 0 (Interleukins); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-21); 147205-72-9 (CD40 Ligand); 148971-36-2 (Ikaros Transcription Factor); EC 3.4.- (CRBN protein, human); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601725


  8 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28829194
[Au] Autor:Mao H; Pan F; Wu Z; Wang Z; Zhou Y; Zhang P; Gou M; Dai G
[Ad] Endereço:1 Department of Oncology, Chinese PLA General Hospital , Bejing, China .
[Ti] Título:CD19 CD27 Plasmablasts Suppress Harmful Th17 Inflammation Through Interleukin 10 Pathway in Colorectal Cancer.
[So] Source:DNA Cell Biol;36(10):870-877, 2017 Oct.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The enrichment of CD20 and CD138 immune cells were previously associated with improved survival in colorectal cancer (CRC). We previously discovered that the resected tumors in CRC patients were highly enriched with interleukin (IL)-10-producing CD19 CD27 plasmablasts with potential suppressor functions. It is still unknown what roles the CD19 CD27 plasmablasts play in CRC patients. In this study, we first demonstrated that B cells from peripheral blood mononuclear cells (PBMCs) could be stimulated to resemble tumor-infiltrating plasmablasts using a coculture containing Caco-2 and heat-killed bacteria. The PBMC-derived CD19 CD27 plasmablasts and tumor-infiltrating plasmablasts contained comparable frequencies of IL-10-expressing cells and secreted similar levels of IL-10. We later found that these CD19 CD27 plasmablasts significantly suppressed the mRNA and cytokine expression of IL-17A in PBMCs, as well as the expression of RAR-related orphan receptor gamma t (RORγt) in CD4 T cells. This suppressive effect did not involve the induction of Foxp3 regulatory T cells, since no upregulation of Foxp3 level was observed. Through IL-10/IL-10R blocking and exogenous IL-10 experiments, we found that these CD19 CD27 plasmablasts primarily mediated IL-17A suppression through IL-10 production. Other B cell-related mechanisms might also contribute to this inhibitory effect. In our cohort of patients, patients with high frequency of tumor-infiltrating IL-10 CD19 CD27 plasmablasts presented low IL-17A CD4 T cell frequency and better survival. Altogether, these results suggested that CD19 CD27 plasmablasts with Breg functions were associated with better prognosis in CRC, possibly by suppressing harmful Th17 inflammation.
[Mh] Termos MeSH primário: Linfócitos B Reguladores/imunologia
Linfócitos T CD4-Positivos/metabolismo
Neoplasias Colorretais/metabolismo
Interleucina-10/metabolismo
Plasmócitos/metabolismo
Células Th17/imunologia
[Mh] Termos MeSH secundário: Antígenos CD19/imunologia
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
Interleucina-17/imunologia
Linfócitos T Reguladores/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD19 molecule, human); 0 (IL10 protein, human); 0 (IL17A protein, human); 0 (Interleukin-17); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 130068-27-8 (Interleukin-10)
[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:170823
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3814


  9 / 1585 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28809949
[Au] Autor:Svensson A; Patzi Churqui M; Schlüter K; Lind L; Eriksson K
[Ad] Endereço:Department of Rheumatology and Inflammation Research, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
[Ti] Título:Maturation-dependent expression of AIM2 in human B-cells.
[So] Source:PLoS One;12(8):e0183268, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intracellular DNA- and RNA-sensing receptors, such as the IFN-inducible protein Absent in Melanoma 2 (AIM2), serve as host sensors against a wide range of infections. Immune sensing and inflammasome activation by AIM2 has been implicated in innate antiviral recognition in many experimental systems using cell-lines and animal models. However, little is known about the expression and function of AIM2 in freshly isolated human cells. In this study we investigated the expression of AIM2 in different cell types derived from human cord and adult peripheral blood, in steady state and following in vitro-activation. Adult but not cord blood B-cells expressed high levels of AIM2 mRNA at steady state. In adults, AIM2 was primarily expressed in mature memory CD27+ B-cells. Both adult and cord blood derived B-cells could induce their transcription of AIM2 mRNA in response to type II IFN but not type I IFN or the AIM2 ligand poly dA:dT. Upon B-cell receptor stimulation, B-cells from adult blood expressed reduced levels of AIM2 mRNA. In addition, we show that adult B-cells were able to release IL-1ß upon stimulation with synthetic DNA. We conclude that functional AIM2 is preferentially expressed in adult human CD27+ B-cells, but is absent in cord blood mononuclear cells.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Proteínas de Ligação a DNA/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Células Cultivadas
Proteínas de Ligação a DNA/genética
Citometria de Fluxo
Seres Humanos
Interleucina-1alfa/metabolismo
Interleucina-1beta/metabolismo
Leucócitos Mononucleares/metabolismo
RNA Mensageiro/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIM2 protein, human); 0 (DNA-Binding Proteins); 0 (Interleukin-1alpha); 0 (Interleukin-1beta); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7)
[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:170816
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183268


  10 / 1585 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28710252
[Au] Autor:Collin R; St-Pierre C; Guilbault L; Mullins-Dansereau V; Policheni A; Guimont-Desrochers F; Pelletier AN; Gray DH; Drobetsky E; Perreault C; Hillhouse EE; Lesage S
[Ad] Endereço:Department of Immunology-Oncology, Maisonneuve-Rosemont Hospital, Montreal, Quebec H1T 2M4, Canada.
[Ti] Título:An Unbiased Linkage Approach Reveals That the p53 Pathway Is Coupled to NK Cell Maturation.
[So] Source:J Immunol;199(4):1490-1504, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer cells constitute potent innate lymphoid cells that play a major role in both tumor immunosurveillance and viral clearance via their effector functions. A four-stage model of NK cell functional maturation has been established according to the expression of CD11b and CD27, separating mature NK (mNK) cells into distinct populations that exhibit specific phenotypic and functional properties. To identify genetic factors involved in the regulation of NK cell functional maturation, we performed a linkage analysis on F (B6.Rag1 × NOD.Rag1 intercross) mice. We identified six loci on chromosomes 2, 4, 7, 10, 11, and 18 that were linked to one or more mNK cell subsets. Subsequently, we performed an in silico analysis exploiting mNK cell subset microarray data, highlighting various genes and microRNAs as potential regulators of the functional maturation of NK cells. Together, the combination of our unbiased genetic linkage study and the in silico analysis positions genes known to affect NK cell biology along the specific stages of NK cell functional maturation. Moreover, this approach allowed us to uncover a novel candidate gene in the regulation of NK cell maturation, namely Using mice deficient for , we confirm that this tumor suppressor regulates NK cell functional maturation. Additional candidate genes revealed in this study may eventually serve as targets for the modulation of NK cell functional maturation to potentiate both tumor immunosurveillance and viral clearance.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Ligação Genética
Células Matadoras Naturais/fisiologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/imunologia
Diferenciação Celular
Processos de Crescimento Celular
Células Cultivadas
Simulação por Computador
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/imunologia
Células Matadoras Naturais/imunologia
Camundongos
Camundongos Endogâmicos NOD
MicroRNAs/genética
MicroRNAs/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Homeodomain Proteins); 0 (MicroRNAs); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (Tumor Suppressor Protein p53); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600789



página 1 de 159 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde