Base de dados : MEDLINE
Pesquisa : D12.644.276.374.750.656 [Categoria DeCS]
Referências encontradas : 496 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 50 ir para página                         

  1 / 496 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  2 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  3 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28911883
[Au] Autor:McWilliams TG; Howard L; Wyatt S; Davies AM
[Ad] Endereço:Division of Molecular Biosciences, School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, United Kingdom.
[Ti] Título:TNF superfamily member APRIL enhances midbrain dopaminergic axon growth and contributes to the nigrostriatal projection in vivo.
[So] Source:Exp Neurol;298(Pt A):97-103, 2017 Dec.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have studied the role of the tumor necrosis factor superfamily member APRIL in the development of embryonic mouse midbrain dopaminergic neurons in vitro and in vivo. In culture, soluble APRIL enhanced axon growth during a window of development between E12 and E14 when nigrostriatal axons are growing to their targets in the striatum in vivo. April transcripts were detected in both the striatum and midbrain during this period and at later stages. The axon growth-enhancing effect of APRIL was similar to that of glial cell-derived neurotrophic factor (GDNF), but in contrast to GDNF, APRIL did not promote the survival of midbrain dopaminergic neurons. The effect of APRIL on axon growth was prevented by function-blocking antibodies to one of its receptors, BCMA (TNFRSF13A), but not by function-blocking antibodies to the other APRIL receptor, TACI (TNFRSF13B), suggesting that the effects of APRIL on axon growth are mediated by BCMA. In vivo, there was a significant reduction in the density of midbrain dopaminergic projections to the striatum in April-/- embryos compared with wild type littermates at E14. These findings demonstrate that APRIL is a physiologically relevant factor for the nigrostriatal projection. Given the importance of the degeneration of dopaminergic nigrostriatal connections in the pathogenesis and progression of Parkinson's disease, our findings contribute to our understanding of the factors that establish nigrostriatal integrity.
[Mh] Termos MeSH primário: Axônios/fisiologia
Corpo Estriado/fisiologia
Neurônios Dopaminérgicos/fisiologia
Mesencéfalo/fisiologia
Substância Negra/fisiologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Células Cultivadas
Corpo Estriado/efeitos dos fármacos
Neurônios Dopaminérgicos/efeitos dos fármacos
Relação Dose-Resposta a Droga
Mesencéfalo/efeitos dos fármacos
Camundongos
Camundongos Knockout
Substância Negra/efeitos dos fármacos
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tnfsf13 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[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:170916
[St] Status:MEDLINE


  4 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28383107
[Au] Autor:Haselmayer P; Vigolo M; Nys J; Schneider P; Hess H
[Ad] Endereço:Department of Immunopharmacology, Immunology Translational Innovation Platform, Merck KGaA, Darmstadt, Germany.
[Ti] Título:A mouse model of systemic lupus erythematosus responds better to soluble TACI than to soluble BAFFR, correlating with depletion of plasma cells.
[So] Source:Eur J Immunol;47(6):1075-1085, 2017 Jun.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The TNF family cytokines B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) support plasma cell survival. It is known that inhibitors of BAFF only (BAFFR-Fc) or BAFF and APRIL (TACI-Fc) administered early enough in an NZB/NZW F1 mouse model of systemic lupus erythematosus (SLE) ameliorate clinical outcomes, pointing to a pathogenic role of BAFF. In the present study, TACI-Fc administrated at a later stage of disease, after onset of autoimmunity, decreased the number of bone marrow plasma cells and slowed down further formation of autoantibodies. TACI-Fc prevented renal damage during a 12-week treatment period regardless of autoantibody levels, while BAFFR-Fc did not despite a similar BAFF-blocking activity in vivo. TACI-Fc also decreased established plasma cells in a T-dependent hapten/carrier immunization system better than single inhibitors of BAFF or APRIL, and sometimes better than combined single inhibitors with at least equivalent BAFF and APRIL inhibitory activities. These results indicate that TACI-Fc can prevent symptoms of renal damage in a mouse model of SLE when BAFFR-Fc cannot, and point to a plasticity of plasma cells for survival factors. Targeting plasma cells with TACI-Fc might be beneficial to prevent autoantibody-mediated damages in SLE.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Lúpus Eritematoso Sistêmico/imunologia
Plasmócitos/imunologia
Proteína Transmembrana Ativadora e Interagente do CAML/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/biossíntese
Autoimunidade
Fator Ativador de Células B/antagonistas & inibidores
Fator Ativador de Células B/imunologia
Receptor do Fator Ativador de Células B/administração & dosagem
Receptor do Fator Ativador de Células B/imunologia
Linfócitos B/imunologia
Citometria de Fluxo
Rim/imunologia
Rim/patologia
Lúpus Eritematoso Sistêmico/fisiopatologia
Lúpus Eritematoso Sistêmico/terapia
Camundongos
Plasmócitos/patologia
Proteína Transmembrana Ativadora e Interagente do CAML/imunologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/antagonistas & inibidores
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (B-Cell Activating Factor); 0 (B-Cell Activation Factor Receptor); 0 (Tnfrsf13b protein, mouse); 0 (Tnfrsf13c protein, mouse); 0 (Tnfsf13 protein, mouse); 0 (Tnfsf13b protein, mouse); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201746934


  5 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28381397
[Au] Autor:McCarron MJ; Park PW; Fooksman DR
[Ad] Endereço:Department of Pathology, Albert Einstein College of Medicine, Bronx, NY; and.
[Ti] Título:CD138 mediates selection of mature plasma cells by regulating their survival.
[So] Source:Blood;129(20):2749-2759, 2017 May 18.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antibody secreting cells (ASCs) are critical effector cells and long-lived sentinels for immune memory. ASCs are highly dependent on exogenous soluble factors such as interleukin-6 (IL-6) and APRIL, to prevent their cell death. We have found that the canonical surface marker of ASCs, CD138 (syndecan-1), which is upregulated during ASC maturation, is required in a cell-intrinsic manner to mount an effective long-term humoral immune response following immunization. Surface expression of CD138 increased heparan sulfate levels on ASCs, which are known to bind pro-survival cytokines, leading to increased survival in a cell-intrinsic manner in vivo. In IL-6 and APRIL-deficient hosts, ASCs underwent extensive apoptosis independently of CD138 expression. We propose a model in which CD138 expression on fully mature ASCs provides a selective survival advantage over less mature, newly minted ASCs, by enhancing pro-survival cytokine signaling.
[Mh] Termos MeSH primário: Diferenciação Celular
Plasmócitos/citologia
Plasmócitos/metabolismo
Sindecana-1/metabolismo
[Mh] Termos MeSH secundário: Animais
Formação de Anticorpos/imunologia
Apoptose
Sobrevivência Celular
Epitopos/imunologia
Centro Germinativo/imunologia
Seres Humanos
Imunidade Humoral
Interleucina-6/metabolismo
Camundongos Endogâmicos C57BL
Transdução de Sinais/imunologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epitopes); 0 (Interleukin-6); 0 (Syndecan-1); 0 (Tnfsf13 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-01-761643


  6 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28323891
[Au] Autor:Granja AG; Holland JW; Pignatelli J; Secombes CJ; Tafalla C
[Ad] Endereço:Centro de Investigación en Sanidad Animal (CISA-INIA). Valdeolmos (Madrid), Spain.
[Ti] Título:Characterization of BAFF and APRIL subfamily receptors in rainbow trout (Oncorhynchus mykiss). Potential role of the BAFF / APRIL axis in the pathogenesis of proliferative kidney disease.
[So] Source:PLoS One;12(3):e0174249, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proliferative kidney disease (PKD) is a parasitic infection of salmonid fish characterized by hyper-secretion of immunoglobulins in response to the presence of the myxozoan parasite, Tetracapsuloides bryosalmonae. In this context, we hypothesized that the BAFF/APRIL axis, known to play a major role in B cell differentiation and survival in mammals, could be affected by the parasite and consequently be involved in the apparent shift in normal B cell activity. To regulate B cell activity, BAFF and APRIL bind to transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) and B cell maturation antigen (BCMA), whereas BAFF also binds to BAFF receptor (BAFF-R). In teleost fish, although some BAFF and APRIL sequences have been reported, their receptors have not been identified. Thus, as a first step in the current work, we have identified homologues to mammalian TACI, BCMA and BAFF-R in rainbow trout (Oncorhynchus mykiss), that constitute the first report of BAFF and APRIL receptor sequences in fish. Subsequently we studied the transcriptional modulation of BAFF, APRIL, and the fish-specific related cytokine, BALM and their putative receptors in fish naturally exposed to T. bryosalmonae. Finally, to gain further insights on the functional role that these cytokines play during the course of PKD, we have studied their effect on the survival of kidney IgM+ B cells and on immunoglobulin transcription. Our results support the premise that the BAFF / APRIL axis could play an important role during PKD, which may open the possibility of new therapeutic treatments against the disease.
[Mh] Termos MeSH primário: Receptor do Fator Ativador de Células B/metabolismo
Antígeno de Maturação de Linfócitos B/metabolismo
Doenças dos Peixes/patologia
Nefropatias/patologia
Oncorhynchus mykiss/parasitologia
Doenças Parasitárias em Animais/patologia
Proteína Transmembrana Ativadora e Interagente do CAML/metabolismo
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Sequência de Bases
Doenças dos Peixes/parasitologia
Regulação da Expressão Gênica
Nefropatias/parasitologia
Myxozoa
Doenças Parasitárias em Animais/parasitologia
Análise de Sequência de DNA
Proteína Transmembrana Ativadora e Interagente do CAML/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activation Factor Receptor); 0 (B-Cell Maturation Antigen); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174249


  7 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28302579
[Au] Autor:Soleto I; Abós B; Castro R; González L; Tafalla C; Granja AG
[Ad] Endereço:Centro de Investigación en Sanidad Animal (CISA-INIA), Madrid, Spain.
[Ti] Título:The BAFF / APRIL axis plays an important role in virus-induced peritoneal responses in rainbow trout.
[So] Source:Fish Shellfish Immunol;64:210-217, 2017 May.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:IgM B cells have been recently demonstrated to be key regulators of peritoneal inflammation in teleost, as a large number of them occupy the peritoneal cavity after 48 h of antigenic stimulation. Despite this, the number of studies addressing the mechanism through which this cell population expands and differentiates in response to stimuli has been scarcely addressed. Because the BAFF/APRIL axis is known to play a major role in B cell survival and differentiation in mammals, we hypothesized that it could be affected in the peritoneal cavity in response to an inflammatory stimulus. To verify this hypothesis, we studied how BAFF, APRIL and the fish-specific related cytokine BALM as well as their putative receptors are regulated in rainbow trout after intraperitoneal (i.p.) injection of viral hemorrhagic septicemia virus (VHSV). When the transcriptional analysis was performed in total cells from the peritoneum, we observed that VHSV provoked an up-regulation of both BAFF and BAFF receptor (BAFF-R) mRNA levels. However, when we examined how isolated peritoneal IgM B cells were transcriptionally affected by VHSV i.p. injection, we found that APRIL, BALM and the transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) were also up-regulated in response to the virus. IgM cells, on the other hand, only up-regulated BALM transcription in response to VHSV. Finally, to gain further insight on the role that these cytokines play in the peritoneum, we have studied their effect on the survival of peritoneal IgM B cells. This work demonstrates a key role for the BAFF/APRIL axis in the peritoneal inflammatory response and contributes to further understanding how IgM B cells are regulated at this specific peripheral site.
[Mh] Termos MeSH primário: Doenças dos Peixes/genética
Proteínas de Peixes/genética
Novirhabdovirus/fisiologia
Oncorhynchus mykiss
Infecções por Rhabdoviridae/veterinária
[Mh] Termos MeSH secundário: Animais
Receptor do Fator Ativador de Células B/genética
Receptor do Fator Ativador de Células B/metabolismo
Linfócitos B/imunologia
Citocinas/genética
Citocinas/metabolismo
Doenças dos Peixes/imunologia
Doenças dos Peixes/virologia
Proteínas de Peixes/metabolismo
Peritônio/fisiopatologia
Peritônio/virologia
Infecções por Rhabdoviridae/genética
Infecções por Rhabdoviridae/imunologia
Infecções por Rhabdoviridae/virologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activation Factor Receptor); 0 (Cytokines); 0 (Fish Proteins); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170628
[Lr] Data última revisão:
170628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


  8 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28284352
[Au] Autor:Deng B; Liu XN; Li X; Zhang X; Quan C; Chen XJ
[Ad] Endereço:Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China.
[Ti] Título:Raised cerebrospinal fluid BAFF and APRIL levels in anti-N-methyl-d-aspartate receptor encephalitis: Correlation with clinical outcome.
[So] Source:J Neuroimmunol;305:84-91, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In this study, we aimed to assess the levels of B cell activating factor from the tumor necrosis factor family (BAFF) and a proliferation-inducing ligand (APRIL) in cerebrospinal fluid (CSF) of patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis and determine their correlation with clinical outcome. BAFF and APRIL concentrations in CSF and serum from 40 patients with anti-NMDAR encephalitis and 20 controls were measured by enzyme-linked immunosorbent assay (ELISA). Compared with controls, the levels of both BAFF and APRIL in CSF were significantly increased in patients with anti-NMDAR encephalitis (p<0.001 and p<0.001). Patients with unfavorable outcome had higher levels of BAFF and APRIL in CSF than those who had favorable outcome (p<0.05 and p<0.05). BAFF and APRIL levels in CSF were elevated and associated with clinical outcome in patients with anti-NMDAR encephalitis, indicating that they may be valuable biomarkers to this disease.
[Mh] Termos MeSH primário: Encefalite Antirreceptor de N-Metil-D-Aspartato/líquido cefalorraquidiano
Fator Ativador de Células B/líquido cefalorraquidiano
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Adolescente
Adulto
Encefalite Antirreceptor de N-Metil-D-Aspartato/complicações
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Estudos Longitudinais
Masculino
Meia-Idade
Neoplasias Ovarianas/complicações
Estudos Retrospectivos
Índice de Gravidade de Doença
Estatística como Assunto
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


  9 / 496 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28267197
[Au] Autor:Tran NL; Schneider P; Santiago-Raber ML
[Ad] Endereço:Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
[Ti] Título:TACI-dependent APRIL signaling maintains autoreactive B cells in a mouse model of systemic lupus erythematosus.
[So] Source:Eur J Immunol;47(4):713-723, 2017 Apr.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Autoantibodies contribute to the development of systemic lupus erythematosus (SLE). APRIL (a proliferation-inducing ligand), a member of the TNF superfamily, regulates plasma-cell survival and binds to TACI (transmembrane activator CAML interactor) and BCMA (B-cell maturation antigen). We previously showed that APRIL blockade delayed disease onset in lupus-prone mice. In order to evaluate the role of APRIL receptors in the development of SLE, APRIL, TACI, BCMA, or double TACI.BCMA null mutations were introduced into the Nba2.Yaa (Y-linked autoimmune acceleration) spontaneous lupus mouse model. Mortality as a consequence of glomerulonephritis (GN) was reduced in Nba2.APRIL .Yaa, Nba2.TACI .Yaa and double-KO mice compared with Nba2.Yaa mice and correlated with lower levels of circulating antibodies, while splenic populations remained unchanged. In contrast, the appearance of symptoms was accelerated in BCMA-deficient mice, in which TACI signaling was increased. Finally, lupus-prone mice deficient for the APRIL-TACI axis produced less pathogenic antibodies and developed less GN. Disease reduction was attributed to impaired T-independent type 2 responses when the APRIL-TACI signaling axis was disrupted. Collectively, our results have identified and confirmed APRIL as a new target involved in B-cell activation, in the maintenance of plasma cell survival and subsequent increased autoantibody production that sustains lupus development in mice.
[Mh] Termos MeSH primário: Antígeno de Maturação de Linfócitos B/metabolismo
Linfócitos B/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Proteína Transmembrana Ativadora e Interagente do CAML/metabolismo
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/metabolismo
Autoantígenos/imunologia
Antígeno de Maturação de Linfócitos B/genética
Células Cultivadas
Modelos Animais de Doenças
Suscetibilidade a Doenças
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Mutantes
Transdução de Sinais/genética
Proteína Transmembrana Ativadora e Interagente do CAML/genética
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (B-Cell Maturation Antigen); 0 (Tnfrsf13b protein, mouse); 0 (Tnfrsf17 protein, mouse); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646630


  10 / 496 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28260502
[Au] Autor:Zheng C; Zhang X; Zhao Z; Hao X; Wei J; Sun J
[Ad] Endereço:Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300072, China.
[Ti] Título:Selective Binding BAFF/APRIL by the In and Outside Conservative Region of BCMA.
[So] Source:Protein Pept Lett;24(6):489-494, 2017.
[Is] ISSN:1875-5305
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: BAFF and APRIL are members of TNF superfamily. They play vital roles in the pathogenesis of autoimmune diseases. BCMA, a receptor, shows higher affinity for APRIL than for BAFF. Previous studies found that ligand binding specificity of BCMA may be determined by sequence outside DxL motif. OBJECTIVE: Investigate the contribution of a segment outside the DxL motif of BCMA for binding with ligands. METHOD: In this study, the conservative region of BCMA was divided into two segments: BCMA1 (NEYFDSLLHACIPC), a segment of the DXL motif and BCMA2 (QLRCSSNTPPLT), a segment outside of the DXL motif. Two peptides corresponding to the two segments were synthesized and their contribution to the ligands binding were detected by competitive ELISA. BCMA1-Fc fusion protein was also constructed, purified and analyzed by indirect and competitive ELISA. RESULTS: BCMA2 had no inhibiting effect on the interaction of BCMA-Fc and BCMA1-Fc with BAFF, but, it inhibited 22.5% and 15.2% of the interaction of BCMA-Fc and BCMA1-Fc with mAPRIL respectively. The binding rates of BCMA1-Fc for BAFF were 91.7%, but 80.6% for mAPRIL, suggesting that BCMA1-Fc without BCMA2, bound BAFF well and less efficiently to mAPRIL. CONCLUSION: These results suggest that BCMA2 outside of the conservative DxL motif of BCMA may play an important role in the binding selectivity to its ligands.
[Mh] Termos MeSH primário: Fator Ativador de Células B/genética
Antígeno de Maturação de Linfócitos B/genética
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Fator Ativador de Células B/química
Antígeno de Maturação de Linfócitos B/química
Sequência Conservada/genética
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Ligantes
Ligação Proteica
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (B-Cell Maturation Antigen); 0 (Ligands); 0 (TNFRSF17 protein, human); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE
[do] DOI:10.2174/0929866524666170301115209



página 1 de 50 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