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1.
J Immunol ; 175(1): 182-8, 2005 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-15972646

RESUMO

Both CD28 and ICOS are important costimulatory molecules that promote Ag-specific cellular and humoral immune reactions. Whereas CD28 is generally thought to be the most important molecule in the initiation of a T cell response, ICOS is considered to act during the effector phase. We have investigated the contribution of ICOS to T cell responses in the absence of CTLA-4-mediated inhibition. Mice lacking CTLA-4, which show spontaneous CD28-mediated CD4(+) T cell activation, expansion and differentiation, were treated with antagonistic alphaICOS antibodies. Blocking the interaction between ICOS and its ligand B7RP-1 significantly reduced this aberrant T cell activation and caused a reduction in T cell numbers. In vitro analysis of CD4(+) T cells from treated mice revealed that ICOS blockade significantly reduced Th1 differentiation, while Th2 differentiation was only moderately inhibited. Further in vitro stimulation experiments demonstrated that ICOS is able to induce proliferation of murine CD4(+) and CD8(+) T cells but only in the presence of IL-2. These results indicate that ICOS is not only important for T cell effector function but also contributes to the expansion phase of a T cell response in the presence of CD28 signaling.


Assuntos
Antígenos de Diferenciação de Linfócitos T/metabolismo , Antígenos de Diferenciação/metabolismo , Linfócitos T/imunologia , Animais , Antígenos CD , Antígenos de Diferenciação/genética , Antígenos CD28/metabolismo , Antígeno CTLA-4 , Diferenciação Celular , Proliferação de Células/efeitos dos fármacos , Técnicas In Vitro , Proteína Coestimuladora de Linfócitos T Induzíveis , Interleucina-2/farmacologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Transdução de Sinais , Subpopulações de Linfócitos T/citologia , Subpopulações de Linfócitos T/efeitos dos fármacos , Subpopulações de Linfócitos T/imunologia , Linfócitos T/citologia , Linfócitos T/efeitos dos fármacos
2.
Immunity ; 16(2): 157-68, 2002 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-11869678

RESUMO

K/BxN T cell receptor transgenic mice are a model of inflammatory arthritis, similar to rheumatoid arthritis. Disease in these animals is focused specifically on the joints but stems from autoreactivity to a ubiquitously expressed antigen, glucose-6-phosphate isomerase (GPI). T and B cells are both required for disease initiation, but anti-GPI immunoglobulins (Igs), alone, can induce arthritis in lymphocyte-deficient recipients. Here, we show that the arthritogenic Igs act through both Fc receptors (in particular, FcgammaRIII) and the complement network (C5a). Surprisingly, the alternative pathway of complement activation is critical, while classical pathway components are entirely dispensable. We suggest that autoimmune disease, even one that is organ specific, can occur when mobilization of an adaptive immune response results in runaway activation of the innate response.


Assuntos
Artrite Reumatoide/imunologia , Proteínas do Sistema Complemento/imunologia , Receptores de IgG/imunologia , Transdução de Sinais/imunologia , Animais , Antígenos CD/imunologia , Artrite Reumatoide/genética , Proteínas do Sistema Complemento/genética , Modelos Animais de Doenças , Sistema Imunitário , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Knockout , Receptor da Anafilatoxina C5a , Receptores de Complemento/imunologia , Receptores de IgG/genética
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