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Pesquisa : D12.776.395.550.114.500 [Categoria DeCS]
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  1 / 1818 MEDLINE  
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[PMID]:27771353
[Au] Autor:Peng W
[Ad] Endereço:Institute of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong City, Sichuan 637000, P. R. China; Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, Mount Scopus, Sderot Churchill, Jerusalem, 91240, Israel. Electronic address: pengwei39@hotmail.com.
[Ti] Título:G-CSF treatment promotes apoptosis of autoreactive T cells to restrict the inflammatory cascade and accelerate recovery in experimental allergic encephalomyelitis.
[So] Source:Exp Neurol;289:73-84, 2017 03.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G-CSF is a hematopoietic growth factor that regulates the proliferation, differentiation and survival of myeloid lineage cells, which has protective effects in autoimmune neuroinflammatory diseases such as EAE. Here we use EAE model treated by G-CSF to address the hypothesis that G-CSF inhibits the proliferative response of splenic T cells via the enhancement of apoptosis, and this priming effect of G-CSF depends on the cell cycle. Our results show that G-CSF administration reduced EAE frequency and severity of attacks. The inflammatory cells and demyelination areas were decreased in the CNS of G-CSF-treated mice. G-CSF treatment altered cytokine profiles in vivo to inhibit the productions of IFN-γ, IL-1ß, IL-2, TNF-α, IL-17 and NO, while the secretions of IL-4 and IL-10 were increased. Splenic T cells from G-CSF-treated mice showed significantly lower proliferative response to specific antigen MOG stimulation. G-CSF enhanced the percentage of a CD4 CD25 T cell subset in spleen T cells. Moreover, G-CSF promoted the G0/G1 to S phase transition of MOG autoreactive T cells inducing apoptosis and elevating Bax gene expression of apoptosis marker. These findings indicate that G-CSF treatment induces the apoptosis of MOG autoreactive T cells, which decreases the production of pro-inflammatory cytokines and NO, suppresses the proliferation of autoreactive T cells and elevates a CD4 CD25 T cell subset to inhibit inflammatory infiltration and demyelination within CNS of EAE. The conclusions of G-CSF treatment in EAE mice suggest that G-CSF is clinically applicable and may be considered for future use in therapeutic measures for multiple sclerosis treatment.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Linfócitos T CD4-Positivos/efeitos dos fármacos
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/fisiopatologia
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Recuperação de Função Fisiológica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anexina A5/metabolismo
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Feminino
Adjuvante de Freund/toxicidade
Expressão Gênica/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Glicoproteína Mielina-Oligodendrócito/toxicidade
Óxido Nítrico/metabolismo
Fragmentos de Peptídeos/toxicidade
Toxina Pertussis/toxicidade
Baço/patologia
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Cytokines); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (bcl-2-Associated X Protein); 0 (myelin oligodendrocyte glycoprotein (35-55)); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 31C4KY9ESH (Nitric Oxide); 9007-81-2 (Freund's Adjuvant); EC 2.4.2.31 (Pertussis Toxin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 1818 MEDLINE  
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[PMID]:28986408
[Au] Autor:Houzen H; Kondo K; Niino M; Horiuchi K; Takahashi T; Nakashima I; Tanaka K
[Ad] Endereço:From the Department of Neurology (H.H., K.H.), Obihiro Kosei General Hospital, Obihiro; Department of Neurology (K.K.), Hokuto Hospital, Obihiro; Department of Clinical Research (M.N.), Hokkaido Medical Center, Sapporo; Department of Neurology (T.T., I.N.), Tohoku University, Sendai; Department of N
[Ti] Título:Prevalence and clinical features of neuromyelitis optica spectrum disorders in northern Japan.
[So] Source:Neurology;89(19):1995-2001, 2017 Nov 07.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To clarify the prevalence and clinical characteristics of neuromyelitis optica spectrum disorders (NMOSD) in Japan and compare them with those in other ethnic populations. METHODS: Data processing sheets were sent to all related institutions in northern Japan and were collected from April to May 2016. Prevalence was determined on March 31, 2016, using the 2015 International Panel for NMO Diagnosis criteria. RESULTS: The crude prevalence was 4.1/100,000 (95% confidence interval 2.2-6.9) for NMOSD in northern Japan, with a significantly higher number of female than male patients (female: male 12:2). The positivity for anti-aquaporin-4 antibody was 78.6%, and the mean age at onset was 45.2 years. All patients were subjected to preventive therapy in the form of treatment with steroids or immunosuppressive agents. CONCLUSIONS: Our results showed that the prevalence of NMOSD in the Japanese population is similar to that in Caucasians.
[Mh] Termos MeSH primário: Neuromielite Óptica/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Idoso
Aquaporina 4/imunologia
Autoanticorpos/sangue
Avaliação da Deficiência
Grupos Étnicos
Feminino
Inquéritos Epidemiológicos
Seres Humanos
Japão/epidemiologia
Masculino
Meia-Idade
Glicoproteína Mielina-Oligodendrócito/imunologia
Neuromielite Óptica/sangue
Neuromielite Óptica/diagnóstico
Prevalência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 4); 0 (Autoantibodies); 0 (Myelin-Oligodendrocyte Glycoprotein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004611


  3 / 1818 MEDLINE  
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[PMID]:28887429
[Au] Autor:Blanchfield L; Sabatino JJ; Lawrence L; Evavold BD
[Ad] Endereço:Department of Microbiology and Immunology, Emory University, Atlanta, GA 30322.
[Ti] Título:NFM Cross-Reactivity to MOG Does Not Expand a Critical Threshold Level of High-Affinity T Cells Necessary for Onset of Demyelinating Disease.
[So] Source:J Immunol;199(8):2680-2691, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Of interest to the etiology of demyelinating autoimmune disease is the potential to aberrantly activate CD4 T cells due to cross-recognition of multiple self-epitopes such as has been suggested for myelin oligodendrocyte glycoprotein epitope 35-55 (MOG ) and neurofilament medium protein epitope 15-35 (NFM ). NFM is immunogenic in C57BL/6 mice but fails to induce demyelinating disease by polyclonal T cells despite having the same TCR contact residues as MOG , a known encephalitogenic Ag. Despite reported cross-reactivity with MOG-specific T cells, the polyclonal response to NFM did not expand threshold numbers of MOG tetramer-positive T cells. Furthermore, NFM lacked functional synergy with MOG to promote experimental autoimmune encephalomyelitis because NFM-deficient synonymous with knockout mice developed an identical disease course to wild-type mice after challenge with MOG Single-cell analysis of encephalitogenic T cells using the peptide:MHC monomer-based two-dimensional micropipette adhesion frequency assay confirmed that NFM was not a critical Ag driving demyelinating disease because NFM -specific T cells in the CNS were predominantly reactive to MOG The absence of NFM contribution to disease allowed mapping of the amino acids required for encephalitogenicity and expansion of high-affinity, MOG-specific T cells that defined the polyclonal response. Alterations of N-terminal residues outside of the NFM core nonamer promoted expansion of high-affinity, MOG tetramer-positive T cells and promoted consistent experimental autoimmune encephalomyelitis induction, unlike mice challenged with NFM Although NFM is immunogenic and cross-reactive with MOG at the polyclonal level, it fails to expand a threshold level of encephalitogenic, high-affinity MOG-specific T cells.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Reações Cruzadas
Encefalomielite Autoimune Experimental/imunologia
Esclerose Múltipla/imunologia
Receptores de Antígenos de Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Mapeamento de Epitopos
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Glicoproteína Mielina-Oligodendrócito/imunologia
Fragmentos de Peptídeos/imunologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (Receptors, Antigen, T-Cell); 0 (myelin oligodendrocyte glycoprotein (35-55))
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700792


  4 / 1818 MEDLINE  
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[PMID]:28872459
[Au] Autor:Li B; Wang X; Choi IY; Wang YC; Liu S; Pham AT; Moon H; Smith DJ; Rao DS; Boldin MP; Yang L
[Ad] Endereço:Department of Microbiology, Immunology and Molecular Genetics.
[Ti] Título:miR-146a modulates autoreactive Th17 cell differentiation and regulates organ-specific autoimmunity.
[So] Source:J Clin Invest;127(10):3702-3716, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoreactive CD4 T cells that differentiate into pathogenic Th17 cells can trigger autoimmune diseases. Therefore, investigating the regulatory network that modulates Th17 differentiation may yield important therapeutic insights. miR-146a has emerged as a critical modulator of immune reactions, but its role in regulating autoreactive Th17 cells and organ-specific autoimmunity remains largely unknown. Here, we have reported that miR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS). We bred miR-146a-deficient mice with 2D2 T cell receptor-Tg mice to generate 2D2 CD4 T cells that are deficient in miR-146a and specific for myelin oligodendrocyte glycoprotein (MOG), an autoantigen in the EAE model. miR-146a-deficient 2D2 T cells induced more severe EAE and were more prone to differentiate into Th17 cells. Microarray analysis revealed enhancements in IL-6- and IL-21-induced Th17 differentiation pathways in these T cells. Further study showed that miR-146a inhibited the production of autocrine IL-6 and IL-21 in 2D2 T cells, which in turn reduced their Th17 differentiation. Thus, our study identifies miR-146a as an important molecular brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic target for treating autoimmune diseases.
[Mh] Termos MeSH primário: Autoimunidade
Diferenciação Celular/imunologia
Encefalomielite Autoimune Experimental/imunologia
MicroRNAs/imunologia
Esclerose Múltipla/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Animais
Comunicação Autócrina/genética
Comunicação Autócrina/imunologia
Diferenciação Celular/genética
Encefalomielite Autoimune Experimental/genética
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Interleucinas/genética
Interleucinas/imunologia
Camundongos
Camundongos Knockout
MicroRNAs/genética
Esclerose Múltipla/genética
Glicoproteína Mielina-Oligodendrócito/genética
Glicoproteína Mielina-Oligodendrócito/imunologia
Especificidade de Órgãos/genética
Especificidade de Órgãos/imunologia
Células Th17/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Interleukins); 0 (MicroRNAs); 0 (Mirn146 microRNA, mouse); 0 (Mog protein, mouse); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (interleukin-21); 0 (interleukin-6, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


  5 / 1818 MEDLINE  
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[PMID]:28848043
[Au] Autor:Young KE; Flaherty S; Woodman KM; Sharma-Walia N; Reynolds JM
[Ad] Endereço:Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
[Ti] Título:Fatty acid synthase regulates the pathogenicity of Th17 cells.
[So] Source:J Leukoc Biol;102(5):1229-1235, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T cell activation and effector function is characterized by changes in metabolism. Altered metabolism is common to almost all types of activated T cells, but fatty acid synthesis seems to especially drive the formation of Th17 cells. Indeed, research has demonstrated that inhibition of early fatty acid synthesis through targeting of acetyl-CoA carboxylase (ACC1) can inhibit Th17 cell formation and instead promote the generation of regulatory T cells. Fatty acid synthase (FASN) is downstream of ACC, and previous studies have shown that FASN activity influences both cancer and inflammation. However, it remains to be determined whether FASN is a viable target for inhibiting Th17 cell function. Here, we demonstrate that FASN is a critical metabolic control for the generation of inflammatory subsets of Th17 cells. Conversely, inhibiting FASN function promotes IFN-γ production by Th1 and Th1-like Th17 cells. In vivo, inhibition of FASN, specifically in Th17 cells, leads to reduction of experimental autoimmune encephalomyelitis disease. These studies demonstrate the necessity of FASN in the autoimmune inflammatory function of Th17 cells.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/imunologia
Ácido Graxo Sintase Tipo I/imunologia
Interferon gama/imunologia
Interleucina-17/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: 4-Butirolactona/análogos & derivados
4-Butirolactona/farmacologia
Animais
Diferenciação Celular
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/genética
Inibidores Enzimáticos/farmacologia
Ácido Graxo Sintase Tipo I/antagonistas & inibidores
Ácido Graxo Sintase Tipo I/genética
Regulação da Expressão Gênica
Seres Humanos
Interferon gama/genética
Interleucina-17/genética
Interleucina-23/genética
Interleucina-23/imunologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Glicoproteína Mielina-Oligodendrócito
Fragmentos de Peptídeos
Cultura Primária de Células
Transdução de Sinais
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/patologia
Células Th1/efeitos dos fármacos
Células Th1/imunologia
Células Th1/patologia
Células Th17/efeitos dos fármacos
Células Th17/patologia
Receptor 2 Toll-Like/genética
Receptor 2 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-methylene-2-octyl-5-oxofuran-3-carboxylic acid); 0 (Enzyme Inhibitors); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 0 (myelin oligodendrocyte glycoprotein (35-55)); 82115-62-6 (Interferon-gamma); EC 2.3.1.85 (Fatty Acid Synthase, Type I); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3AB0417-159RR


  6 / 1818 MEDLINE  
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[PMID]:28789840
[Au] Autor:Huang ZL; Pandya D; Banta DK; Ansari MS; Oh U
[Ad] Endereço:Department of Neurology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
[Ti] Título:Cyclophilin inhibitor NIM811 ameliorates experimental allergic encephalomyelitis.
[So] Source:J Neuroimmunol;311:40-48, 2017 Oct 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cyclophilins have diverse functions that may affect the course of central nervous system (CNS) inflammatory disorders. Anti-inflammatory and neuroprotective mechanisms may be targeted by inhibition of cyclophilin A-dependent and cyclophilin D-dependent functions, respectively. We tested the effect of cyclophilin inhibition on CNS inflammation by administering N-methyl-4-isoleucine-cyclosporin (NIM811) to mice undergoing experimental allergic encephalomyelitis (EAE). Treatment with NIM811 resulted in significant reduction of EAE clinical severity. Analysis of mitochondrial calcium retention capacity and the course of EAE in cyclophilin D knockout mice indicated that the effect of NIM811 on EAE was not entirely cyclophilin D-dependent. NIM811-treated EAE animals showed reduction in interleukin-2 expression and reduction in CNS inflammatory infiltrates. These results indicate that anti-inflammatory rather than neuroprotective mechanisms associated with cyclophilins are likely involved in the mechanism of NIM811 in EAE.
[Mh] Termos MeSH primário: Ciclosporina/uso terapêutico
Encefalomielite Autoimune Experimental/tratamento farmacológico
Imunossupressores/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/ultraestrutura
Calcineurina/metabolismo
Cálcio/metabolismo
Ciclofilinas/deficiência
Ciclofilinas/genética
Ciclosporina/metabolismo
Ciclosporina/farmacologia
Citocinas/genética
Citocinas/metabolismo
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/patologia
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Imunossupressores/farmacologia
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microglia/efeitos dos fármacos
Microglia/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Glicoproteína Mielina-Oligodendrócito/imunologia
Glicoproteína Mielina-Oligodendrócito/toxicidade
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/toxicidade
Baço/metabolismo
Baço/ultraestrutura
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Immunosuppressive Agents); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (myelin oligodendrocyte glycoprotein (35-55)); 83HN0GTJ6D (Cyclosporine); 96262S4I14 ((melle-4)cyclosporin); EC 3.1.3.16 (Calcineurin); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (cyclophilin D); SY7Q814VUP (Calcium)
[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:170810
[St] Status:MEDLINE


  7 / 1818 MEDLINE  
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[PMID]:28778445
[Au] Autor:Benedek G; Zhang J; Nguyen H; Kent G; Seifert HA; Davin S; Stauffer P; Vandenbark AA; Karstens L; Asquith M; Offner H
[Ad] Endereço:Neuroimmunology Research, VA Portland Health Care System, 3710 SW U.S. Veterans Hospital Rd, Portland, OR 97239, USA; Department of Neurology, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA.
[Ti] Título:Estrogen protection against EAE modulates the microbiota and mucosal-associated regulatory cells.
[So] Source:J Neuroimmunol;310:51-59, 2017 Sep 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sex hormones promote immunoregulatory effects on multiple sclerosis. In the current study we evaluated the composition of the gut microbiota and the mucosal-associated regulatory cells in estrogen or sham treated female mice before and after autoimmune encephalomyelitis (EAE) induction. Treatment with pregnancy levels of estrogen induces changes in the composition and diversity of gut microbiota. Additionally, estrogen prevents EAE-associated changes in the gut microbiota and might promote the enrichment of bacteria that are associated with immune regulation. Our results point to a possible cross-talk between the sex hormones and the gut microbiota, which could promote neuroprotection.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/tratamento farmacológico
Estrogênios/uso terapêutico
Intestinos/microbiologia
Microbiota/efeitos dos fármacos
Membrana Mucosa/efeitos dos fármacos
Membrana Mucosa/patologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/patologia
Fezes/microbiologia
Feminino
Interleucina-10/genética
Interleucina-10/metabolismo
Intestinos/efeitos dos fármacos
Leucócitos/efeitos dos fármacos
Linfonodos/efeitos dos fármacos
Linfonodos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Glicoproteína Mielina-Oligodendrócito/toxicidade
Fragmentos de Peptídeos/toxicidade
RNA Ribossômico 16S/genética
RNA Ribossômico 16S/metabolismo
Medula Espinal/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Estrogens); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (RNA, Ribosomal, 16S); 0 (myelin oligodendrocyte glycoprotein (35-55)); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170826
[Lr] Data última revisão:
170826
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE


  8 / 1818 MEDLINE  
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[PMID]:28768844
[Au] Autor:Hennes EM; Baumann M; Schanda K; Anlar B; Bajer-Kornek B; Blaschek A; Brantner-Inthaler S; Diepold K; Eisenkölbl A; Gotwald T; Kuchukhidze G; Gruber-Sedlmayr U; Häusler M; Höftberger R; Karenfort M; Klein A; Koch J; Kraus V; Lechner C; Leiz S; Leypoldt F; Mader S; Marquard K; Poggenburg I; Pohl D; Pritsch M; Raucherzauner M; Schimmel M; Thiels C; Tibussek D; Vieker S; Zeches C; Berger T; Reindl M; Rostásy K; BIOMARKER Study Group
[Ad] Endereço:Author affiliations are provided at the end of the article.
[Ti] Título:Prognostic relevance of MOG antibodies in children with an acquired demyelinating syndrome.
[So] Source:Neurology;89(9):900-908, 2017 Aug 29.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To assess the prognostic value of MOG antibodies (abs) in the differential diagnosis of acquired demyelinating syndromes (ADS). METHODS: Clinical course, MRI, MOG-abs, AQP4-abs, and CSF cells and oligoclonal bands (OCB) in children with ADS and 24 months of follow-up were reviewed in this observational prospective multicenter hospital-based study. RESULTS: Two hundred ten children with ADS were included and diagnosed with acute disseminated encephalomyelitis (ADEM) (n = 60), neuromyelitis optica spectrum disorder (NMOSD) (n = 12), clinically isolated syndrome (CIS) (n = 101), and multiple sclerosis (MS) (n = 37) after the first episode. MOG-abs were predominantly found in ADEM (57%) and less frequently in NMOSD (25%), CIS (25%), or MS (8%). Increased MOG-ab titers were associated with younger age ( = 0.0001), diagnosis of ADEM ( = 0.005), increased CSF cell counts ( = 0.011), and negative OCB ( = 0.012). At 24-month follow-up, 96 children had no further relapses. Thirty-five children developed recurrent non-MS episodes (63% MOG-, 17% AQP4-abs at onset). Seventy-nine children developed MS (4% MOG-abs at onset). Recurrent non-MS episodes were associated with high MOG-ab titers ( = 0.0003) and older age at onset ( = 0.024). MS was predicted by MS-like MRI ( < 0.0001) and OCB ( = 0.007). An MOG-ab cutoff titer ≥1:1,280 predicted a non-MS course with a sensitivity of 47% and a specificity of 100% and a recurrent non-MS course with a sensitivity of 46% and a specificity of 86%. CONCLUSIONS: Our results show that the presence of MOG-abs strongly depends on the age at disease onset and that high MOG-ab titers were associated with a recurrent non-MS disease course.
[Mh] Termos MeSH primário: Encefalomielite Aguda Disseminada/imunologia
Esclerose Múltipla/imunologia
Glicoproteína Mielina-Oligodendrócito/sangue
Glicoproteína Mielina-Oligodendrócito/imunologia
Neuromielite Óptica/imunologia
[Mh] Termos MeSH secundário: Adolescente
Autoanticorpos
Biomarcadores/metabolismo
Criança
Pré-Escolar
Diagnóstico Diferencial
Progressão da Doença
Encefalomielite Aguda Disseminada/sangue
Encefalomielite Aguda Disseminada/líquido cefalorraquidiano
Encefalomielite Aguda Disseminada/diagnóstico por imagem
Feminino
Seguimentos
Seres Humanos
Lactente
Imagem por Ressonância Magnética
Masculino
Esclerose Múltipla/sangue
Esclerose Múltipla/líquido cefalorraquidiano
Esclerose Múltipla/diagnóstico por imagem
Neuromielite Óptica/sangue
Neuromielite Óptica/líquido cefalorraquidiano
Neuromielite Óptica/diagnóstico por imagem
Bandas Oligoclonais
Prognóstico
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (MOG protein, human); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Oligoclonal Bands)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004312


  9 / 1818 MEDLINE  
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[PMID]:28759648
[Au] Autor:Ip FCF; Ng YP; Or TCT; Sun P; Fu G; Li JYH; Ye WC; Cheung TH; Ip NY
[Ad] Endereço:Division of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
[Ti] Título:Anemoside A3 ameliorates experimental autoimmune encephalomyelitis by modulating T helper 17 cell response.
[So] Source:PLoS One;12(7):e0182069, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Anemoside A3 (AA3) is a natural triterpenoid glycoside isolated from the root of Pulsatilla chinensis (Bunge) Regel. We previously showed that AA3 exhibits cognitive-enhancing and neuroprotective properties. In the present study, we demonstrated that AA3 modulates inflammatory responses by regulating prostaglandin E receptor 4 signaling. Because prostaglandin E receptor 4 is involved in the pathophysiology of experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), we assessed the beneficial effect of AA3 in EAE mice. AA3 treatment significantly reduced clinical severity and inflammatory infiltrates in the spinal cord of EAE mice. In vitro studies revealed that AA3 inhibited the T cell response toward the encephalitogenic epitope of myelin oligodendrocyte glycoprotein (MOG). AA3 significantly downregulated the expressions of certain Th1 and Th17 cytokines in activated T cells re-stimulated by MOG. Moreover, AA3 inhibited the activation of STAT4 and STAT3, which are the transcription factors pivotal for Th1 and Th17 lineage differentiation, respectively, in activated T cells. Pharmacological analysis further suggested that AA3 reduced Th17 cell differentiation and expansion. In conclusion, AA3 exerts an immunomodulatory effect in EAE, demonstrating its potential as a therapeutic agent for MS in humans.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/tratamento farmacológico
Saponinas/uso terapêutico
Células Th17/efeitos dos fármacos
Triterpenos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Linhagem Celular Tumoral
Células Cultivadas
Citocinas/metabolismo
Encefalomielite Autoimune Experimental/imunologia
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Glicoproteína Mielina-Oligodendrócito/genética
Glicoproteína Mielina-Oligodendrócito/metabolismo
Fator de Transcrição STAT3/metabolismo
Fator de Transcrição STAT4/metabolismo
Saponinas/farmacologia
Medula Espinal/efeitos dos fármacos
Medula Espinal/imunologia
Medula Espinal/patologia
Células Th17/citologia
Células Th17/imunologia
Triterpenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Mog protein, mouse); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (STAT3 Transcription Factor); 0 (STAT4 Transcription Factor); 0 (Saponins); 0 (Stat3 protein, mouse); 0 (Stat4 protein, mouse); 0 (Triterpenes); 0 (anemoside A3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182069


  10 / 1818 MEDLINE  
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[PMID]:28684532
[Au] Autor:Hyun JW; Woodhall MR; Kim SH; Jeong IH; Kong B; Kim G; Kim Y; Park MS; Irani SR; Waters P; Kim HJ
[Ad] Endereço:Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Korea.
[Ti] Título:Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases.
[So] Source:J Neurol Neurosurg Psychiatry;88(10):811-817, 2017 Oct.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We evaluated the seroprevalence of myelin oligodendrocyte glycoprotein immunoglobulin G1 (MOG-IgG) and associated clinical features of patients from a large adult-dominant unselected cohort with mainly relapsing central nervous system (CNS) inflammatory diseases. We also investigate the clinical relevance of MOG-IgG through a longitudinal analysis of serological status over a 2-year follow-up period. METHODS: Serum samples from 505 patients with CNS inflammatory diseases at the National Cancer Center were analysed using cell-based assays for MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG). MOG-IgG serostatus was longitudinally assessed in seropositive patients with available serum samples and at least 2 years follow-up. RESULTS: Twenty-two of 505 (4.4%) patients with CNS inflammatory diseases were positive for MOG-IgG. Patients with MOG-IgG had neuromyelitis optica spectrum disorder (NMOSD, n=10), idiopathic AQP4-IgG-negative myelitis (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3) and multiple sclerosis (n=1). No relapses were seen in patients when they became MOG-IgG seronegative, whereas a persistent positive serological status was observed in patients with clinical relapses despite immunotherapy. CONCLUSIONS: In a large adult-predominant unselected cohort of mainly relapsing CNS inflammatory diseases, we confirmed that NMOSD phenotype was most commonly observed in patients with MOG-IgG. A longitudinal analysis with 2-year follow-up suggested that persistence of MOG-IgG is associated with relapses.
[Mh] Termos MeSH primário: Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central
Glicoproteína Mielina-Oligodendrócito/imunologia
Estudos Soroepidemiológicos
[Mh] Termos MeSH secundário: Aquaporina 4/imunologia
Autoanticorpos/imunologia
Doenças Autoimunes Desmielinizantes do Sistema Nervoso Central/sangue
Seres Humanos
Imunoglobulina G/sangue
Estudos Longitudinais
Imagem por Ressonância Magnética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 4); 0 (Autoantibodies); 0 (Immunoglobulin G); 0 (Myelin-Oligodendrocyte Glycoprotein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2017-315998



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