Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Pathog Dis ; 72(1): 61-9, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24833344

RESUMO

Two hallmarks of advanced atherosclerosis are calcification and fibrosis. We hypothesized that Chlamydia pneumoniae infection may contribute to atherosclerosis by inducing the conversion of vascular smooth muscle cells to calcifying cells or by converting mesenchymal stem cells to osteochondrocytic or fibroblastic phenotypes. In this study, direct infection of bovine aortic smooth muscle cells (BSMCs) did not induce the expression of alkaline phosphatase or the deposition of extracellular calcium phosphate. However, conditioned media from C. pneumoniae-infected macrophages accelerated conversion of BSMCs to a calcifying phenotype. Treatment of the conditioned media with an anti-TNF-alpha blocking antibody abrogated this stimulatory effect. Treatment of perivascular Sca-1+, CD31-, CD45- cells from apoE-/- mouse aortas with the conditioned media from infected macrophages induced the Sca-1+ cells to produce collagen II, an additional marker of an osteochondrocytic phenotype. Treatment of mouse coronary perivascular Sca-1+, CD31-, CD45- cells with the supernatant from homogenates of C. pneumoniae-infected mouse lungs as compared to noninfected lungs induced expression of the Collagen 1α1 gene and deposition of collagen. Therefore, an increase in plasma cytokines or other factors in response to respiratory infection with C. pneumoniae or infection of macrophages within the blood vessel could contribute to both calcification and fibrosis of advanced atherosclerotic lesions.


Assuntos
Infecções por Chlamydia/patologia , Chlamydophila pneumoniae/fisiologia , Fibrose , Pulmão/microbiologia , Macrófagos/microbiologia , Células-Tronco Mesenquimais/patologia , Miócitos de Músculo Liso/patologia , Calcificação Vascular , Animais , Bovinos , Células Cultivadas , Meios de Cultivo Condicionados , Modelos Animais de Doenças , Pulmão/patologia , Macrófagos/imunologia , Camundongos Endogâmicos C57BL
2.
J Immunol ; 178(2): 887-96, 2007 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-17202350

RESUMO

The pathogenesis of multiple sclerosis involves a breakdown in T cell tolerance to myelin proteins like myelin basic protein (MBP). Most MBP-specific T cells are eliminated by central tolerance in adult mice, however, the developmentally regulated expression of MBP allows MBP-specific thymocytes in young mice to escape negative selection. It is not known how these T cells that encounter MBP for the first time in the periphery are regulated. We show that naive MBP-specific T cells transferred into T cell-deficient mice induce severe autoimmunity. Regulatory T cells prevent disease, however, suppression of the newly transferred MBP-specific T cells is abrogated by activating APCs in vivo. Without APC activation, MBP-specific T cells persist in the periphery of protected mice but do not become anergic, raising the question of how long-term tolerance can be maintained if APCs presenting endogenous MBP become activated. Our results demonstrate that regulatory T cells induce naive MBP-specific T cells responding to nonactivated APCs to differentiate into a unique, tolerized state with the ability to produce IL-10 and TGF-beta1 in response to activated, but not nonactivated, APCs presenting MBP. This tolerant response depends on continuous activity of regulatory T cells because, in their absence, these uniquely tolerized MBP-specific T cells can again induce autoimmunity.


Assuntos
Tolerância Imunológica/imunologia , Proteína Básica da Mielina/metabolismo , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/metabolismo , Animais , Células Apresentadoras de Antígenos/imunologia , Autoimunidade/imunologia , Proliferação de Células , Sistema Nervoso Central/citologia , Sistema Nervoso Central/imunologia , Citocinas/biossíntese , Fatores de Transcrição Forkhead/metabolismo , Transfusão de Linfócitos , Camundongos , Camundongos Transgênicos , Proteína Básica da Mielina/deficiência , Proteína Básica da Mielina/genética , Proteína Básica da Mielina/imunologia , Baço/citologia , Baço/imunologia , Linfócitos T Reguladores/citologia , Células Th1/imunologia , Células Th1/metabolismo , Fatores de Tempo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...