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[PMID]: 27776452 [Au] Autor: Vo Ngoc DT; Krist L; van Overveld FJ; Rijkers GT [Ad] Endereço: a Department of Science , University College Roosevelt , Middelburg , The Netherlands. [Ti] Título: The long and winding road to IgA deficiency: causes and consequences. [So] Source: Expert Rev Clin Immunol;13(4):371-382, 2017 04. [Is] ISSN: 1744-8409 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: INTRODUCTION: The most common humoral immunodeficiency is IgA deficiency. One of the first papers addressing the cellular and molecular mechanisms underlying IgA deficiency indicated that immature IgA-positive B-lymphocytes are present in these patients. This suggests that the genetic background for IgA is still intact and that class switching can take place. At this moment, it cannot be ruled out that genetic as well as environmental factors are involved. Areas covered: A clinical presentation, the biological functions of IgA, and the management of IgA deficiency are reviewed. In some IgA deficient patients, a relationship with a loss-of-function mutation in the TACI (transmembrane activator and calcium-modulating cyclophilin ligand interaction) gene has been found. Many other genes also have been associated. Gut microbiota are an important environmental trigger for IgA synthesis. Expert commentary: Expression of IgA deficiency is due to both genetic and environmental factors and a role for gut microbiota cannot be excluded. [Mh] Termos MeSH primário: Linfócitos B/fisiologia Deficiência de IgA/imunologia Imunidade nas Mucosas Imunoglobulina A/metabolismo Microbiota/imunologia Células Precursoras de Linfócitos B/fisiologia Proteína Transmembrana Ativadora e Interagente do CAML/genética [Mh] Termos MeSH secundário: Animais Fator Ativador de Células B/genética Interação Gene-Ambiente Predisposição Genética para Doença Seres Humanos Deficiência de IgA/etiologia Switching de Imunoglobulina Polimorfismo Genético Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (B-Cell Activating Factor); 0 (Immunoglobulin A); 0 (TNFRSF13B protein, human); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 180215 [Lr] Data última revisão: 180215 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161026 [St] Status: MEDLINE [do] DOI: 10.1080/1744666X.2017.1248410

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[PMID]: 28461109 [Au] Autor: Amrouche K; Jamin C [Ad] Endereço: UMR 1227, Lymphocytes B et Autoimmunité, Université de Brest, INSERM, Brest, France; LabEx IGO "Immunotherapy, Graft, Oncology", Brest, France. [Ti] Título: Influence of drug molecules on regulatory B cells. [So] Source: Clin Immunol;184:1-10, 2017 11. [Is] ISSN: 1521-7035 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: By their suppressive functions, regulatory B (Breg) cells are considered as key elements in the control and development of various disease states. Many signals can induce Bregs in vivo and in vitro and often from heterogeneous populations. Several specific signals delivered in a timely immunological context contribute to the establishment of Bregs. These are endogenous and physiological signals or stimuli, widely discussed in the literature participating in the establishment of an effective immune response. However, exogenous signals, much less clearly identified can also be considered as Bregs inducers. These extrinsic signals are capable of directly or indirectly influencing the suppressive capacity of Bregs, but also their expansion and functional restoration in its absence. Faced with the excitement generated by the development of processes favoring the expansion of Bregs in mice for therapeutic purposes, the challenge today is to extrapolate such approaches in humans. This perspective may already be in effect. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Linfócitos B Reguladores/efeitos dos fármacos Imunossupressores/farmacologia Vitaminas/farmacologia [Mh] Termos MeSH secundário: Corticosteroides/farmacologia Animais Anticorpos Monoclonais Humanizados/farmacologia Fator Ativador de Células B/imunologia Linfócitos B Reguladores/imunologia Antígenos CD40/imunologia Citocinas/imunologia Seres Humanos Metotrexato/farmacologia Ácido Micofenólico/farmacologia Pirróis/farmacologia Quinazolinas/farmacologia Receptores de Antígenos de Linfócitos B/imunologia Semaforinas/farmacologia Sirolimo/farmacologia Receptores Toll-Like/imunologia Tretinoína/farmacologia Vitamina D/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Adrenal Cortex Hormones); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (B-Cell Activating Factor); 0 (CD40 Antigens); 0 (Cytokines); 0 (Immunosuppressive Agents); 0 (Pyrroles); 0 (Quinazolines); 0 (Receptors, Antigen, B-Cell); 0 (Semaphorins); 0 (Toll-Like Receptors); 0 (Vitamins); 1406-16-2 (Vitamin D); 5688UTC01R (Tretinoin); 7I279E1NZ8 (sotrastaurin); HU9DX48N0T (Mycophenolic Acid); I031V2H011 (tocilizumab); W36ZG6FT64 (Sirolimus); YL5FZ2Y5U1 (Methotrexate) [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

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[PMID]: 28300280 [Au] Autor: Zeng Q; Qin S; Zhang H; Liu B; Qin J; Wang X; Zhang R; Liu C; Dong X; Zhang S; Huang S; Chen L [Ad] Endereço: Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, Nanjing, PR China. [Ti] Título: Rapamycin attenuates BAFF-extended proliferation and survival via disruption of mTORC1/2 signaling in normal and neoplastic B-lymphoid cells. [So] Source: J Cell Physiol;233(1):516-529, 2018 Jan. [Is] ISSN: 1097-4652 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: B cell activating factor from the TNF family (BAFF) stimulates B-cell proliferation and survival, but excessive BAFF promotes the development of aggressive B cells leading to malignant and autoimmune diseases. Recently, we have reported that rapamycin, a macrocyclic lactone, attenuates human soluble BAFF (hsBAFF)-stimulated B-cell proliferation/survival by suppressing mTOR-mediated PP2A-Erk1/2 signaling pathway. Here, we show that the inhibitory effect of rapamycin on hsBAFF-promoted B cell proliferation/survival is also related to blocking hsBAFF-stimulated phosphorylation of Akt, S6K1, and 4E-BP1, as well as expression of survivin in normal and B-lymphoid (Raji and Daudi) cells. It appeared that both mTORC1 and mTORC2 were involved in the inhibitory activity of rapamycin, as silencing raptor or rictor enhanced rapamycin's suppression of hsBAFF-induced survivin expression and proliferation/viability in B cells. Also, PP242, an mTORC1/2 kinase inhibitor, repressed survivin expression, and cell proliferation/viability more potently than rapamycin (mTORC1 inhibitor) in B cells in response to hsBAFF. Of interest, ectopic expression of constitutively active Akt (myr-Akt) or constitutively active S6K1 (S6K1-ca), or downregulation of 4E-BP1 conferred resistance to rapamycin's attenuation of hsBAFF-induced survivin expression and B-cell proliferation/viability, whereas overexpression of dominant negative Akt (dn-Akt) or constitutively hypophosphorylated 4E-BP1 (4EBP1-5A), or downregulation of S6K1, or co-treatment with Akt inhibitor potentiated the inhibitory effects of rapamycin. The findings indicate that rapamycin attenuates excessive hsBAFF-induced cell proliferation/survival via blocking mTORC1/2 signaling in normal and neoplastic B-lymphoid cells. Our data underscore that rapamycin may be a potential agent for preventing excessive BAFF-evoked aggressive B-cell malignancies and autoimmune diseases. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Fator Ativador de Células B/metabolismo Linfócitos B/efeitos dos fármacos Proliferação Celular/efeitos dos fármacos Linfoma de Células B/tratamento farmacológico Complexos Multiproteicos/metabolismo Transdução de Sinais/efeitos dos fármacos Sirolimo/farmacologia Serina-Treonina Quinases TOR/metabolismo [Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética Proteínas Adaptadoras de Transdução de Sinal/metabolismo Linfócitos B/enzimologia Linfócitos B/patologia Linhagem Celular Tumoral Sobrevivência Celular/efeitos dos fármacos Relação Dose-Resposta a Droga Regulação Neoplásica da Expressão Gênica Seres Humanos Linfoma de Células B/genética Linfoma de Células B/patologia Alvo Mecanístico do Complexo 1 de Rapamicina Alvo Mecanístico do Complexo 2 de Rapamicina Fosfoproteínas/genética Fosfoproteínas/metabolismo Fosforilação Proteínas Proto-Oncogênicas c-akt/genética Proteínas Proto-Oncogênicas c-akt/metabolismo Interferência de RNA Proteínas Quinases S6 Ribossômicas 70-kDa/genética Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo Transfecção [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Adaptor Proteins, Signal Transducing); 0 (Antineoplastic Agents); 0 (B-Cell Activating Factor); 0 (EIF4EBP1 protein, human); 0 (Multiprotein Complexes); 0 (Phosphoproteins); 0 (TNFSF13B protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa); EC 2.7.11.1 (ribosomal protein S6 kinase, 70kD, polypeptide 1); W36ZG6FT64 (Sirolimus) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171212 [Lr] Data última revisão: 171212 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170317 [St] Status: MEDLINE [do] DOI: 10.1002/jcp.25913

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[PMID]: 28463395 [Au] Autor: de la Varga Martínez R; Rodríguez-Bayona B; Añez GA; Medina Varo F; Pérez Venegas JJ; Brieva JA; Rodríguez C [Ad] Endereço: Unidad de Investigación, Hospital Universitario Puerta del Mar (HUPM), Cádiz. [Ti] Título: Clinical relevance of circulating anti-ENA and anti-dsDNA secreting cells from SLE patients and their dependence on STAT-3 activation. [So] Source: Eur J Immunol;47(7):1211-1219, 2017 07. [Is] ISSN: 1521-4141 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Disturbances of plasma cell homeostasis and auto-antibody production are hallmarks of systemic lupus erythematosus. The aim of this study was to explore the presence of circulating anti-ENA and anti-dsDNA antibody-secreting cells, to determine their dependence on plasma cell-niche cytokines and to analyze their clinical value. The study was performed in SLE patients with serum anti-ENA and/or anti-dsDNA antibodies (n = 57). Enriched B-cell fractions and sorted antibody-secreting cells (CD19 CD38 ) were obtained from blood. dsDNA- and ENA-specific antibody-secreting cells were identified as cells capable of active auto-antibody production in culture. The addition of a combination of IL-6, IL-21, BAFF, APRIL, and CXCL12 to the cultures significantly augmented auto-antibody production and antibody-secreting cell proliferation, whereas it diminished apoptosis. The effect on auto-antibody production was dependent on STAT-3 activation as it was abrogated in the presence of the JAK/STAT-3 pathway inhibitors ruxolitinib and stattic. Among patients with serum anti-dsDNA antibodies, the detection of circulating anti-dsDNA-antibody-secreting cells was associated with higher disease activity markers. In conclusion, auto-antibody production in response to plasma cell-niche cytokines that are usually at high levels in SLE patients is dependent on JAK/STAT-3 activation. Thus, patients with circulating anti-dsDNA antibody-secreting cells and active disease could potentially benefit from therapies targeting the JAK/STAT3 pathway. [Mh] Termos MeSH primário: Anticorpos Antinucleares/sangue Células Produtoras de Anticorpos/imunologia DNA/imunologia Lúpus Eritematoso Sistêmico/imunologia Fator de Transcrição STAT3/metabolismo [Mh] Termos MeSH secundário: Adolescente Adulto Idoso Anticorpos Antinucleares/imunologia Células Produtoras de Anticorpos/efeitos dos fármacos Apoptose/efeitos dos fármacos Fator Ativador de Células B/farmacologia Proliferação Celular Quimiocina CXCL2/farmacologia Óxidos S-Cíclicos/farmacologia DNA/sangue Feminino Seres Humanos Interleucina-6/farmacologia Interleucinas/farmacologia Lúpus Eritematoso Sistêmico/sangue Masculino Meia-Idade Pirazóis/farmacologia Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antibodies, Antinuclear); 0 (B-Cell Activating Factor); 0 (CXCL2 protein, human); 0 (Chemokine CXCL2); 0 (Cyclic S-Oxides); 0 (INCB018424); 0 (Interleukin-6); 0 (Interleukins); 0 (Pyrazoles); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13); 0 (interleukin-21); 0 (stattic); 9007-49-2 (DNA) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 171202 [Lr] Data última revisão: 171202 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170503 [St] Status: MEDLINE [do] DOI: 10.1002/eji.201646872

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[PMID]: 28923901 [Au] Autor: Stohl HE; Lee RH; Manetta J; Kikly K; Korst LM; Stohl W [Ad] Endereço: From the Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA (H.E.S.); Department of Obstetrics and Gynecology (R.H.L.) and Division of Rheumatology, Department of Medicine (W.S.), Los Angeles County+University of Southern Cal [Ti] Título: Maternal Serum B-Cell Activating Factor Levels: Candidate Early Biomarker for Hypertensive Disorders of Pregnancy. [So] Source: Hypertension;70(5):1007-1013, 2017 Nov. [Is] ISSN: 1524-4563 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Hypertensive disorders of pregnancy are a leading cause of maternal and perinatal morbidity and mortality. Early suppression of B-cell lymphopoiesis is necessary for a normal pregnancy. Dysregulation of factors critical to B-cell survival may result in pregnancy complications, including hypertension. In this prospective observational study at a single medical center, serum levels of BAFF (B-cell activating factor) were measured in pregnant participants at each trimester, at delivery, and postpartum and in nonpregnant controls at a single time point. Comparisons were made between nonpregnant and pregnant subjects and between time periods of pregnancy. First-trimester serum BAFF levels were further tested for association with hypertensive disorders of pregnancy. The study included 149 healthy pregnant women, 25 pregnant women with chronic hypertension, and 48 nonpregnant controls. Median first-trimester serum BAFF level (ng/mL) for healthy women (0.90) was lower than median serum BAFF levels for women with chronic hypertension (0.96; =0.013) and controls (1.00; =0.002). Serum BAFF levels steadily declined throughout pregnancy, with the median second-trimester level lower than the corresponding first-trimester level (0.77; =0.003) and the median third-trimester level lower than the corresponding second-trimester level (0.72; =0.025). The median first-trimester serum BAFF level was elevated in women who subsequently developed hypertension compared with women who remained normotensive (1.02 versus 0.85; =0.012), with the area under the receiver operating characteristic curve being 0.709. First-trimester serum BAFF level may be an early and clinically useful predictor of hypertensive disorders of pregnancy. [Mh] Termos MeSH primário: Fator Ativador de Células B/sangue Hipertensão Complicações Cardiovasculares na Gravidez Trimestres da Gravidez/sangue [Mh] Termos MeSH secundário: Adulto Linfócitos B/fisiologia California/epidemiologia Diagnóstico Precoce Feminino Seres Humanos Hipertensão/sangue Hipertensão/diagnóstico Hipertensão/epidemiologia Linfopoese/fisiologia Valor Preditivo dos Testes Gravidez Complicações Cardiovasculares na Gravidez/sangue Complicações Cardiovasculares na Gravidez/diagnóstico Curva ROC Estatística como Assunto [Pt] Tipo de publicação: JOURNAL ARTICLE; OBSERVATIONAL STUDY [Nm] Nome de substância: 0 (B-Cell Activating Factor) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171020 [Lr] Data última revisão: 171020 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170920 [St] Status: MEDLINE [do] DOI: 10.1161/HYPERTENSIONAHA.117.09775

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[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

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[PMID]: 28583852 [Au] Autor: Omachi S; Fujii W; Azuma N; Morimoto A; Sanjoba C; Matsumoto Y; Goto Y [Ad] Endereço: Laboratory of Molecular Immunology, Department of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Japan. [Ti] Título: B-cell activating factor deficiency suppresses splenomegaly during Leishmania donovani infection. [So] Source: Biochem Biophys Res Commun;489(4):528-533, 2017 Aug 05. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: B-cell activating factor (BAFF) is a critical regulator for B-cell development and differentiation. We previously reported elevation of serum BAFF levels in patients with visceral leishmaniasis (VL). In this study, we examined if BAFF is involved in pathologies during infection of Leishmania donovani. BALB/cA mice infected with L. donovani showed significant elevation in serum BAFF and IgG levels as seen in VL patients. In contrast, elevation of serum IgG by L. donovani infection was significantly suppressed in BAFF-deficient mice. The spleen weight of the BAFF-deficient mice after infection was significantly lower than that of the infected wild-type mice, whereas comparable degree of hepatomegaly and anemia were observed in those mice. In the enlarged spleen of L. donovani-infected wild-type mice, increase of CD19 lymphocytes was more prominent than that of CD3 cells, suggesting the contribution of B cell increase to splenomegaly during VL. Besides, increase of CD19 lymphocytes was not found in BAFF-deficient mice after L. donovani infection. Taken together, these results suggest that BAFF is involved in strong B cell activation, which has a pathological role in splenomegaly but not in hepatomegaly or anemia, during VL. [Mh] Termos MeSH primário: Fator Ativador de Células B/deficiência Fator Ativador de Células B/imunologia Leishmania donovani/imunologia Leishmaniose Visceral/imunologia Esplenomegalia/imunologia [Mh] Termos MeSH secundário: Animais Camundongos Camundongos Endogâmicos BALB C Esplenomegalia/parasitologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (B-Cell Activating Factor); 0 (Tnfsf13b protein, mouse) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170922 [Lr] Data última revisão: 170922 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170607 [St] Status: MEDLINE

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[PMID]: 28550073 [Au] Autor: Schneider C; Wunderlich G; Bleistein J; Fink GR; Deckert M; Brunn A; Lehmann HC [Ad] Endereço: Department of Neurology, University of Cologne, Köln, Germany. [Ti] Título: Lymphocyte antigens targetable by monoclonal antibodies in non-systemic vasculitic neuropathy. [So] Source: J Neurol Neurosurg Psychiatry;88(9):756-760, 2017 Sep. [Is] ISSN: 1468-330X [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: OBJECTIVE: To identify the most relevant antigens for monoclonal antibodies in lymphocytic infiltrates in non-systemic vasculitic neuropathy (NSVN). BACKGROUND: Current immunosuppressive treatment for NSVN is insufficient. Monoclonal antibodies might be a treatment option, but the expression profile for targetable antigens on lymphocytic infiltrates in NSVN is unknown. METHODS: Sural nerve biopsies from a cohort of patients with NSVN were immunohistochemically studied for the expression of potential candidate antigens in perivascular and intramural lymphocytic infiltrates and correlated with neurological and electrophysiological parameters. 20 patients with treatment naïve NSVN and 5 patients with idiopathic axonal neuropathy were included. RESULTS: The CD52, BAFF and CD49d antigens were expressed in epineurial, perivascular or intramural lymphocytes of all (20/20) patients. CD52 was most prominently expressed in 21.49% of all inflammatory infiltrates. BAFF and CD49d were detected in 11.25% and 10.99% of these lymphocytes, respectively. The CD20, CD25 and CD126 antigens were found less frequently and at low levels only (CD20: 10/20 patients, 5.84% of lymphocytes; CD25: 17/20 patients, 5.22% of lymphocytes; CD126: 3/20 patients, 0.15% of lymphocytes). CONCLUSION: This is the first study in NSVN that identifies antigens expressed by pathogenic lymphocytes, which are potential targets for future monoclonal antibody treatment. Our data suggest that NSVN is amenable to monoclonal antibodies and, moreover, that targeting CD52 may be particularly promising. Our results strongly warrant future clinical trials in NSVN with monoclonal antibodies. [Mh] Termos MeSH primário: Anticorpos Monoclonais Doenças do Sistema Nervoso Periférico/patologia Nervo Sural/patologia [Mh] Termos MeSH secundário: Idoso Antígenos CD/análise Antígenos de Neoplasias/análise Fator Ativador de Células B/análise Antígeno CD52 Glicoproteínas/análise Seres Humanos Inflamação/patologia Integrina alfa4/análise Meia-Idade Estudos Retrospectivos Vasculite/complicações Vasculite/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (B-Cell Activating Factor); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 0 (TNFSF13B protein, human); 143198-26-9 (Integrin alpha4) [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: 170528 [St] Status: MEDLINE [do] DOI: 10.1136/jnnp-2017-315878

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[PMID]: 28485798 [Au] Autor: Gao XJ; Qu YY; Liu XW; Zhu M; Ma CY; Jiao YL; Cui B; Chen ZJ; Zhao YR [Ad] Endereço: Center of Laboratory Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. y_rzhao@sina.com. [Ti] Título: Immune complexes induce TNF-α and BAFF production from U937 cells by HMGB1 and RAGE. [So] Source: Eur Rev Med Pharmacol Sci;21(8):1810-1819, 2017 Apr. [Is] ISSN: 2284-0729 [Cp] País de publicação: Italy [La] Idioma: eng [Ab] Resumo: OBJECTIVE: This study investigated the effects of immune complexes (ICs) on tumor necrosis factor α (TNF-α) and B cell-activating factor (BAFF) production from U937 cells and further explored the mechanism. MATERIALS AND METHODS: U937 cells were incubated with necrosis supernatant or systemic lupus erythematosus (SLE) sera alone, or their combination. The expression of TNF-α and BAFF was determined by Real-time polymerase chain reaction and enzyme-linked immunosorbent assay. High mobility group box protein 1(HMGB1) A-box was produced by gene recombination. HMGB1 A-box and anti-receptor for advanced glycation end products (RAGE) antibody were adopted in the blocking experiments. The importance of DNA for cytokine induction was investigated by DNase treatment. RESULTS: The combination of necrosis supernatant and SLE sera induced the expression of TNF-α and BAFF significantly increased compared to necrosis supernatant or SLE sera alone. Recombinant HMGB1 A-box protein was purified, and TNF-α and BAFF production, which were induced by this combination, was blocked via HMGB1 A-box and anti-RAGE antibody. Moreover, we found that DNA component is important for the immunostimulatory activity of this combination. CONCLUSIONS: ICs containing DNA can promote TNF-α and BAFF production in U937 cells, and this process can be mediated by HMGB1 and RAGE. One possible mechanism of increasing BAFF production in SLE is proposed in this study whereby B cell activation, antibody production and ICs stimulated monocytes may create a vicious cycle that leads to B cell hyperactivity, which can be of importance for SLE etiopathogenesis. [Mh] Termos MeSH primário: Complexo Antígeno-Anticorpo Antígenos de Neoplasias/metabolismo Fator Ativador de Células B/metabolismo Proteína HMGB1/metabolismo Proteínas Quinases Ativadas por Mitógeno/metabolismo Fator de Necrose Tumoral alfa/metabolismo [Mh] Termos MeSH secundário: Seres Humanos Lúpus Eritematoso Sistêmico/sangue Células U937 [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antigen-Antibody Complex); 0 (Antigens, Neoplasm); 0 (B-Cell Activating Factor); 0 (HMGB1 Protein); 0 (HMGB1 protein, human); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor-alpha); EC 2.7.11.22 (MOK protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinases) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 170731 [Lr] Data última revisão: 170731 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170510 [St] Status: MEDLINE

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[PMID]: 28476436 [Au] Autor: Teos LY; Alevizos I [Ad] Endereço: Sjögren's Syndrome and Salivary Gland Dysfunction Unit, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. [Ti] Título: Genetics of Sjögren's syndrome. [So] Source: Clin Immunol;182:41-47, 2017 Sep. [Is] ISSN: 1521-7035 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The pathogenesis of Sjögren's syndrome has not been elucidated. There has been evidence that genetics play an important role in the development of this disease from earlier studies. However, till now only a number of genes have been identified to be associated with SS, and these have only a weak or moderate effect. In this review we summarize the findings of the genetics studies and emphasize the need of large multicenter projects that will increase the sample sizes to provide more meaningful associations, as is the case in other common autoimmune diseases. [Mh] Termos MeSH primário: Antígenos HLA/genética Síndrome de Sjogren/genética [Mh] Termos MeSH secundário: Fator Ativador de Células B/genética Quimiocina CCL11/genética Proteínas de Ligação a DNA/genética Predisposição Genética para Doença Estudo de Associação Genômica Ampla Seres Humanos Fatores Reguladores de Interferon/genética Subunidade p35 da Interleucina-12/genética Linfotoxina-alfa/genética Receptor 3 Desencadeador da Citotoxicidade Natural/genética Ligante OX40/genética Receptores CXCR5/genética Fator de Transcrição STAT4/genética Proteínas da Membrana Plasmática de Transporte de Serotonina/genética Transativadores/genética Fatores de Transcrição TFII/genética Proteína 3 Induzida por Fator de Necrose Tumoral alfa/genética Quinases da Família src/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (B-Cell Activating Factor); 0 (CCL11 protein, human); 0 (CXCR5 protein, human); 0 (Chemokine CCL11); 0 (DNA-Binding Proteins); 0 (EBF1 protein, human); 0 (GTF2I protein, human); 0 (HLA Antigens); 0 (IL12A protein, human); 0 (IRF5 protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukin-12 Subunit p35); 0 (Lymphotoxin-alpha); 0 (NCR3 protein, human); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (OX40 Ligand); 0 (Receptors, CXCR5); 0 (STAT4 Transcription Factor); 0 (STAT4 protein, human); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (TNFSF13B protein, human); 0 (TNFSF4 protein, human); 0 (TNIP1 protein, human); 0 (Trans-Activators); 0 (Transcription Factors, TFII); EC 2.7.10.2 (BLK protein, human); EC 2.7.10.2 (src-Family Kinases); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171106 [Lr] Data última revisão: 171106 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170507 [St] Status: MEDLINE

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