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[PMID]:28802087
[Au] Autor:Untanu RV; Back J; Appel B; Pei Q; Chen L; Buxton A; Hodgson DC; Ehrlich PF; Constine LS; Schwartz CL; Hutchison RE
[Ad] Endereço:Division of Clinical Pathology, Department of Pathology, State University of New York Upstate Medical University, Syracuse, New York.
[Ti] Título:Variant histology, IgD and CD30 expression in low-risk pediatric nodular lymphocyte predominant Hodgkin lymphoma: A report from the Children's Oncology Group.
[So] Source:Pediatr Blood Cancer;65(1), 2018 Jan.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Histologic prognostic factors have been described for nodular lymphocyte predominant Hodgkin lymphoma (NLPHL). This study examines histologic and immunophenotypic variants in a clinical trial for pediatric NLPHL. PROCEDURE: One hundred sixty-eight cases of localized NLPHL were examined for histologic variants, CD30 and immunoglobulin D (IgD) expression, and outcome. Histologic types were scored categorically as 0 = 0, 1 ≤ 25%, and 2 > 25% of the sample. RESULTS: Fifty-eight (35.1%) cases showed only typical nodular with or without serpiginous histology (types A and B). The remainder showed mixtures of histologies. The numbers of patients with score 2 are 85 (50.6%) type A, 21 (12.5%) type B, 46 (27.4%) with extranodular large B cells (type C), 3 with T-cell-rich nodular pattern (type D), 55 (32.7%) with diffuse T-cell-rich (type E) pattern, and 2 (1.2%) with diffuse B-cell pattern (type F). Higher level of types C (P = 0.048) and D (P = 0.033) resulted in lower event-free survival (EFS). Cytoplasmic IgD was found in 65 of 130 tested (50%), did not significantly associate with EFS but positively correlated with types C and E histology (P < 0.0001) and negatively correlated with types A (P = 0.0003) and B (P = 0.006). Seventeen (10%) expressed CD30, with no adverse effect. CONCLUSIONS: Variant histology is common in pediatric NLPHL, especially types C and E, which are associated with IgD expression. Type C variant histology and possibly type D are associated with decreased EFS, but neither IgD nor CD30 are adverse features. Variant histology may warrant increased surveillance, but did not affect overall survival.
[Mh] Termos MeSH primário: Linfócitos B
Regulação Neoplásica da Expressão Gênica
Doença de Hodgkin
Imunoglobulina D/biossíntese
Antígeno Ki-1/biossíntese
Linfócitos T
[Mh] Termos MeSH secundário: Adolescente
Linfócitos B/metabolismo
Linfócitos B/patologia
Criança
Pré-Escolar
Intervalo Livre de Doença
Feminino
Doença de Hodgkin/metabolismo
Doença de Hodgkin/mortalidade
Doença de Hodgkin/patologia
Seres Humanos
Imuno-Histoquímica
Lactente
Recém-Nascido
Masculino
Taxa de Sobrevida
Linfócitos T/metabolismo
Linfócitos T/patologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Immunoglobulin D); 0 (Ki-1 Antigen)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26753


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[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


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[PMID]:28958373
[Au] Autor:Sokoya M; Ramakrishnan VR; Frank DN; Rahkola J; Getz A; Kingdom TT; Kofonow JM; Nguyen Q; Janoff EN
[Ad] Endereço:Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine, Denver, Colorado.
[Ti] Título:Expression of immunoglobulin D is increased in chronic rhinosinusitis.
[So] Source:Ann Allergy Asthma Immunol;119(4):317-323.e1, 2017 Oct.
[Is] ISSN:1534-4436
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Immunoglobulin (Ig) D is largely localized to the upper airway and reacts with colonizing respiratory pathogens. OBJECTIVE: To determine whether chronic rhinosinusitis (CRS) is associated with increased IgD expression. METHODS: We performed immunofluorescent staining for cytoplasmic IgD, IgA, IgM, and surface plasma cell marker CD138 (syndecan-1) in sinus tissue of patients with CRS with and without nasal polyps (CRSwNP and CRSsNP, respectively) and control subjects without CRS (n = 6 each). Sinonasal mucus antibody levels of patients with CRSwNP or CRSsNP and control subjects were measured by enzyme-linked immunosorbent assay (n = 13, 11, and 9 subjects, respectively). Cells per square millimeter and antibody levels were compared by analysis of variance. Histopathology was performed with sinus tissue from subjects in the 3 groups (n = 6, 8, and 13 subjects respectively). RESULTS: Cells expressing cytoplasmic IgD exceeded those with cytoplasmic IgA and IgM and represented most CD138 plasma cells in the lamina propria. The frequencies of IgD plasma cells were significantly higher in patients with CRSsNP and CRSwNP compared with control subjects (P < .01). Only patients with CRSwNP showed increased frequencies of IgM and IgA plasma cells (P < .01). In contrast to high plasma cell frequencies in tissues, the levels of secreted IgD were lower than those of IgA, IgM, and IgG but were highest in the CRSwNP group compared with the other groups (P < .05). CONCLUSION: IgD plasma cells are prominent in sinus tissues and are increased in CRS. That IgD protein also shows the lowest concentration of antibodies in secretions suggests that its activity might be targeted to the tissue rather than secretions.
[Mh] Termos MeSH primário: Imunoglobulina D/genética
Pólipos Nasais/diagnóstico
Rinite/diagnóstico
Sinusite/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Estudos de Casos e Controles
Doença Crônica
Feminino
Expressão Gênica
Seres Humanos
Imunoglobulina A/genética
Imunoglobulina G/genética
Imunoglobulina M/genética
Masculino
Meia-Idade
Muco/química
Pólipos Nasais/complicações
Pólipos Nasais/genética
Pólipos Nasais/imunologia
Seios Paranasais/imunologia
Seios Paranasais/patologia
Plasmócitos/imunologia
Plasmócitos/patologia
Rinite/complicações
Rinite/genética
Rinite/imunologia
Sinusite/complicações
Sinusite/genética
Sinusite/imunologia
Sindecana-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Immunoglobulin A); 0 (Immunoglobulin D); 0 (Immunoglobulin G); 0 (Immunoglobulin M); 0 (SDC1 protein, human); 0 (Syndecan-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE


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[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


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[PMID]:28832642
[Au] Autor:Lanning DK; Esteves PJ; Knight KL
[Ad] Endereço:Department of Microbiology and Immunology, Center for Translational Research and Education, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, United States of America.
[Ti] Título:The remnant of the European rabbit (Oryctolagus cuniculus) IgD gene.
[So] Source:PLoS One;12(8):e0182029, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although IgD first appeared, along with IgM, in the cartilaginous fishes and has been retained throughout subsequent vertebrate evolution, it has been lost in a diverse group of vertebrate species. We previously showed that, unlike vertebrates that express IgD, the rabbit lacks an IgD (Cδ) gene within 13.5 kb downstream of the IgM gene. We report here that, by conducting BLAST searches of rabbit Ig heavy chain genomic DNA with known mammalian IgD exons, we identified the remnant of the rabbit Cδ gene approximately 21 kb downstream of the IgM gene. The remnant Cδ locus lacks the δCH1 and hinge exons, but contains truncated δCH2 and δCH3 exons, as well as largely intact, but non-functional, secretory and transmembrane exons. In addition, we report that the Cδ gene probably became non-functional in leporids at least prior to the divergence of rabbits and hares ~12 million years ago.
[Mh] Termos MeSH primário: Imunoglobulina D/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Éxons
Filogenia
Coelhos
Homologia de Sequência de Aminoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin D)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182029


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[PMID]:28805811
[Au] Autor:Minguet S; Kläsener K; Schaffer AM; Fiala GJ; Osteso-Ibánez T; Raute K; Navarro-Lérida I; Hartl FA; Seidl M; Reth M; Del Pozo MA
[Ad] Endereço:Department of Immunology, Institute for Biology III, Faculty of Biology, University of Freiburg, Freiburg, Germany.
[Ti] Título:Caveolin-1-dependent nanoscale organization of the BCR regulates B cell tolerance.
[So] Source:Nat Immunol;18(10):1150-1159, 2017 Oct.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Caveolin-1 (Cav1) regulates the nanoscale organization and compartmentalization of the plasma membrane. Here we found that Cav1 controlled the distribution of nanoclusters of isotype-specific B cell antigen receptors (BCRs) on the surface of B cells. In mature B cells stimulated with antigen, the immunoglobulin M BCR (IgM-BCR) gained access to lipid domains enriched for GM1 glycolipids, by a process that was dependent on the phosphorylation of Cav1 by the Src family of kinases. Antigen-induced reorganization of nanoclusters of IgM-BCRs and IgD-BCRs regulated BCR signaling in vivo. In immature Cav1-deficient B cells, altered nanoscale organization of IgM-BCRs resulted in a failure of receptor editing and a skewed repertoire of B cells expressing immunoglobulin-µ heavy chains with hallmarks of poly- and auto-reactivity, which ultimately led to autoimmunity in mice. Thus, Cav1 emerges as a cell-intrinsic regulator that prevents B cell-induced autoimmunity by means of its role in plasma-membrane organization.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Linfócitos B/metabolismo
Caveolina 1/metabolismo
Tolerância Imunológica
Receptores de Antígenos de Linfócitos B/metabolismo
[Mh] Termos MeSH secundário: Animais
Autoimunidade/genética
Autoimunidade/imunologia
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Caveolina 1/genética
Expressão Gênica
Tolerância Imunológica/genética
Imunoglobulina D/imunologia
Imunoglobulina D/metabolismo
Imunoglobulina M/imunologia
Imunoglobulina M/metabolismo
Ativação Linfocitária/genética
Ativação Linfocitária/imunologia
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Fosforilação
Ligação Proteica
Receptores de Antígenos de Linfócitos B/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolin 1); 0 (Immunoglobulin D); 0 (Immunoglobulin M); 0 (Receptors, Antigen, B-Cell)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3813


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[PMID]:28760805
[Au] Autor:Brauner S; Folkersen L; Kvarnström M; Meisgen S; Petersen S; Franzén-Malmros M; Mofors J; Brokstad KA; Klareskog L; Jonsson R; Westerberg LS; Trollmo C; Malmström V; Ambrosi A; Kuchroo VK; Nordmark G; Wahren-Herlenius M
[Ad] Endereço:Department of Medicine, Karolinska University Hosptial, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:H1N1 vaccination in Sjögren's syndrome triggers polyclonal B cell activation and promotes autoantibody production.
[So] Source:Ann Rheum Dis;76(10):1755-1763, 2017 Oct.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Vaccination of patients with rheumatic disease has been reported to result in lower antibody titres than in healthy individuals. However, studies primarily include patients on immunosuppressive therapy. Here, we investigated the immune response of treatment-naïve patients diagnosed with primary Sjögren's syndrome (pSS) to an H1N1 influenza vaccine. METHODS: Patients with Sjögren's syndrome without immunomodulatory treatment and age-matched and gender-matched healthy controls were immunised with an H1N1 influenza vaccine and monitored for serological and cellular immune responses. Clinical symptoms were monitored with a standardised form. IgG class switch and plasma cell differentiation were induced in purified naïve B cells of untreated and hydroxychloroquine-treated patients and healthy controls. Gene expression was assessed by NanoString technology. RESULTS: Surprisingly, treatment-naïve patients with Sjögren's syndrome developed higher H1N1 IgG titres of greater avidity than healthy controls on vaccination. Notably, off-target B cells were also triggered resulting in increased anti-EBV and autoantibody titres. Endosomal toll-like receptor activation of naïve B cells revealed a greater propensity of patient-derived cells to differentiate into plasmablasts and higher production of class switched IgG. The amplified plasma cell differentiation and class switch could be induced in cells from healthy donors by preincubation with type 1 interferon, but was abolished in hydroxychloroquine-treated patients and after in vitro exposure of naïve B cells to chloroquine. CONCLUSIONS: This comprehensive analysis of the immune response in autoimmune patients to exogenous stimulation identifies a mechanistic basis for the B cell hyperactivity in Sjögren's syndrome, and suggests that caution is warranted when considering vaccination in non-treated autoimmune patients.
[Mh] Termos MeSH primário: Anticorpos Antivirais/sangue
Linfócitos B
Citocinas/sangue
Vírus da Influenza A Subtipo H1N1/imunologia
Vacinas contra Influenza/imunologia
Síndrome de Sjogren/imunologia
[Mh] Termos MeSH secundário: Antígenos CD19/análise
Antirreumáticos/farmacologia
Autoanticorpos/biossíntese
Autoantígenos/imunologia
Linfócitos B/química
Linfócitos B/fisiologia
Estudos de Casos e Controles
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Expressão Gênica
Antígenos HLA-DR/análise
Herpesvirus Humano 4/imunologia
Seres Humanos
Hidroxicloroquina/farmacologia
Imunoglobulina D/análise
Imunoglobulina G/sangue
Interferon-alfa/metabolismo
Interferon-alfa/farmacologia
Interleucina-10/farmacologia
Ativação Linfocitária
Contagem de Linfócitos
Ribonucleoproteínas/imunologia
Transdução de Sinais/genética
Síndrome de Sjogren/genética
Receptor 7 Toll-Like/metabolismo
Receptor Toll-Like 9/metabolismo
Transcriptoma
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Antigens, CD19); 0 (Antirheumatic Agents); 0 (Autoantibodies); 0 (Autoantigens); 0 (Cytokines); 0 (HLA-DR Antigens); 0 (Immunoglobulin D); 0 (Immunoglobulin G); 0 (Influenza Vaccines); 0 (Interferon-alpha); 0 (Ribonucleoproteins); 0 (SS-A antigen); 0 (SS-B antigen); 0 (TLR7 protein, human); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 7); 0 (Toll-Like Receptor 9); 130068-27-8 (Interleukin-10); 4QWG6N8QKH (Hydroxychloroquine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-210509


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[PMID]:28626065
[Au] Autor:Torigoe M; Iwata S; Nakayamada S; Sakata K; Zhang M; Hajime M; Miyazaki Y; Narisawa M; Ishii K; Shibata H; Tanaka Y
[Ad] Endereço:First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Fukuoka 807-8555, Japan.
[Ti] Título:Metabolic Reprogramming Commits Differentiation of Human CD27 IgD B Cells to Plasmablasts or CD27 IgD Cells.
[So] Source:J Immunol;199(2):425-434, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B cells play a crucial role in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE). However, the relevance of the metabolic pathway in the differentiation of human B cell subsets remains unknown. In this article, we show that the combination of CpG/TLR9 and IFN-α markedly induced the differentiation of CD27 IgD unswitched memory B cells into CD27 CD38 plasmablasts. The response was accompanied by mammalian target of rapamycin complex 1 (mTORC1) activation and increased lactate production, indicating a shift to glycolysis. However, CpG alone induced the differentiation of unswitched memory B cells into CD27 IgD memory B cells with high cytokine production, but such differentiation was suppressed by IFN-α. AMP-activated protein kinase activation enhanced the differentiation to CD27 IgD B cells, but it attenuated mTORC1 activation and differentiation into plasmablasts. High mTORC1 activation was noted in CD19 B cells of patients with SLE and correlated with plasmablast differentiation and disease activity. Taken together, differential metabolic reprogramming commits the differentiation of human unswitched memory B cells into plasmablasts (the combination of CpG and IFN-α amplifies mTORC1-glycolysis pathways) or CD27 IgD memory B cells (CpG alone amplifies the AMP-activated protein kinase pathway). The former metabolic pathway may play a pivotal role in SLE.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/imunologia
Imunoglobulina D/imunologia
Redes e Vias Metabólicas
Plasmócitos/imunologia
Plasmócitos/fisiologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Subpopulações de Linfócitos B/metabolismo
Linfócitos B/efeitos dos fármacos
Linfócitos B/imunologia
Diferenciação Celular/efeitos dos fármacos
Feminino
Citometria de Fluxo
Seres Humanos
Imunoglobulina D/deficiência
Imunoglobulina D/genética
Memória Imunológica
Imunofenotipagem
Interferon-alfa/imunologia
Ácido Láctico/biossíntese
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Alvo Mecanístico do Complexo 1 de Rapamicina
Redes e Vias Metabólicas/genética
Meia-Idade
Complexos Multiproteicos/genética
Complexos Multiproteicos/metabolismo
Oligodesoxirribonucleotídeos/imunologia
Plasmócitos/metabolismo
Proteínas Quinases/metabolismo
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Receptor Toll-Like 9/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CPG-oligonucleotide); 0 (Immunoglobulin D); 0 (Interferon-alpha); 0 (Multiprotein Complexes); 0 (Oligodeoxyribonucleotides); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 9); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 33X04XA5AT (Lactic Acid); EC 2.7.- (Protein Kinases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601908


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[PMID]:28605137
[Au] Autor:Kubo S; Nakayamada S; Yoshikawa M; Miyazaki Y; Sakata K; Nakano K; Hanami K; Iwata S; Miyagawa I; Saito K; Tanaka Y
[Ad] Endereço:University of Occupational and Environmental Health, Kitakyushu, Japan.
[Ti] Título:Peripheral Immunophenotyping Identifies Three Subgroups Based on T Cell Heterogeneity in Lupus Patients.
[So] Source:Arthritis Rheumatol;69(10):2029-2037, 2017 Oct.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To elucidate the diversity of systemic lupus erythematosus (SLE) based on immunophenotyping. METHODS: Peripheral blood mononuclear cells were obtained from 143 SLE patients and 49 healthy individuals. Circulating B, T, and dendritic cells were defined using flow cytometric analysis as recommended by the Human Immunology Project Consortium. Based on these results, immunophenotypes were distinguished by principal components analysis (PCA), and cluster analysis was used to classify SLE patients into subgroups. RESULTS: The proportions of Treg and follicular helper T (Tfh) cells were higher in SLE patients than in healthy controls, whereas Th1 and Th17 cell proportions did not differ. Proportions of class-switched memory B cells and IgD-CD27- B cells were increased in SLE patients as well. The largest difference compared to the control group was observed in the proportion of plasmablasts, which was higher in SLE patients and correlated with disease activity as assessed with the British Isles Lupus Assessment Group index. PCA indicated that the immunophenotype of SLE patients consisted of abnormalities of the T and B cell axes. Cluster analysis showed that the SLE patients could be stratified into 3 subgroups (with high proportions of plasmablasts in all groups): patients who did not show the characteristic features (T cell-independent group), patients with a high percentage of Tfh cells (Tfh-dominant group), and patients with a high percentage of memory Treg cells (Treg-dominant group). The percentage of patients whose SLE was resistant to treatment was highest among the Tfh-dominant group. CONCLUSION: Our study indicates that patients with active SLE can be divided into 3 subgroups based on T cell heterogeneity. Further immunophenotyping studies should help elucidate the pathogenesis of SLE and provide important information for the development of new therapies.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/imunologia
Linfócitos B/imunologia
Células Dendríticas/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
Células Th1/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Adulto
Análise por Conglomerados
Feminino
Citometria de Fluxo
Seres Humanos
Imunoglobulina D/imunologia
Imunofenotipagem
Masculino
Meia-Idade
Plasmócitos/imunologia
Células Precursoras de Linfócitos B/imunologia
Análise de Componente Principal
Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin D); 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:AIM; IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1002/art.40180


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[PMID]:28603204
[Au] Autor:Yamashita Y; Matsumoto S; Hiramoto R; Komori I; Tanaka T; Nishikomori R; Heike T; Umetsu S; Inui A
[Ad] Endereço:Department of Pediatrics, Matsudo City Hospital Children's Medical Centre.
[Ti] Título:A 6-year-old girl diagnosed with mevalonate kinase deficiency who had hydrops fetalis and neonatal-onset cholestasis.
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(2):131-137, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We experienced a 6-year-old girl diagnosed with mevalonate kinase deficiency (MKD) who had cholestasis, anemia, and elevated inflammatory markers in neonatal period. She was admitted to our hospital because of fever and elevated inflammatory markers at 5 years 11months of age. Without using antibiotics, the fever and the inflammatory markers were spontaneously resolved. MKD was suspected from elevated serum IgD level and the recurrent febrile attacks. The genetic test revealed heterozygous mutation of p.Leu51Phe known as causative gene of MKD and p.Met 282Thr which is the novel mutation. In addition, urinary mevalonate levels increased both in afebrile and febrile periods, and mevalonate kinase activity level was very low. Prednisolone was administered on each attack, and her febrile attack has been controlled well since she was diagnosed with MKD. Fetal edema, cholestasis, anemia, elevation of inflammatory markers in her neonatal period are considered to be complications of MKD. Recurrent fever attacks compromise quality of life in patients with MKD. Children with unexplained cholestasis and anemia in neonatal period, or recurrent fever attacks with elevated inflammatory markers should be examined for MKD.
[Mh] Termos MeSH primário: Colestase/etiologia
Edema/etiologia
Deficiência de Mevalonato Quinase/complicações
Deficiência de Mevalonato Quinase/diagnóstico
[Mh] Termos MeSH secundário: Anemia/etiologia
Biomarcadores/sangue
Biomarcadores/urina
Criança
Feminino
Testes Genéticos
Seres Humanos
Imunoglobulina D/sangue
Deficiência de Mevalonato Quinase/tratamento farmacológico
Deficiência de Mevalonato Quinase/genética
Ácido Mevalônico/urina
Mutação
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Prednisolona/administração & dosagem
Febre Recorrente/etiologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Immunoglobulin D); 9PHQ9Y1OLM (Prednisolone); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.36 (mevalonate kinase); S5UOB36OCZ (Mevalonic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.131



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