Avaliação da imunomodulação de citocinas e componentes apoptoticos por gangliosideos na encefalomielite experimental autoimune

AUTOR(ES)
DATA DE PUBLICAÇÃO

2004

RESUMO

The multiple sclerosis is a chronic inflammatory disease of the central nervous system (SNC), which autoreactive T cells drive immune response against myelin antigens. The relapses and remissions of the disease are responsible for the permanent neurological deficits. The observation of an aberrant inflammatory response against myelin epitopes suggests autoimmune etiology for multiple esclerosis. During the inflammatory process, CD4 T cells activated against myelin antigens cross the blood-brain barrier (BBB) beginning an autoimmune reaction, followed by the release of cytokines, antibodies production and activation of the microglia and astrocytes. By present similarities with the multiple sclerosis, the experimental autoimmune encephalomyelitis (EAE), has been used as experimental model for the study of multiple sclerosis pathology. EAE can be actively induced with myelin proteins, or by infusion of T cells driven against these proteins in the adoptive transfer. As observed in the multiple sclerosis, CD4+T Iymphocytesare the effector cells that release cytokines and recruit other immune cells for the attack to the central nervous system. In this process, cytokines has a crucial role in the EAE modulation, supplying the signs to activate autoreactive T cells. By their neurotrophic and immunomodulatory properties gangliosides have been proposed to reduce deleterious consequences of many neurodegenerative and autoimmune diseases. In the present work, the effects of gangliosides were tested on the switching of Th1 to Th2/Th3 cytokine expression and apoptosis induction, in spleen cells and spinal cord respectively, from Lewis rats on the acute EAE, during clinical signs and after recovery from the disease. The results demonstrate that the group treated with gangliosides show mild disease, with low expression of IFN-gamma mRNA and high TGF-beta mRNA expression, suggestíng that the gangliosides may modulate Th1 cells by the shifting the profile to the Th2/Th3 phenotype. Moreover, the results demonstrate that ganglioside treatment leads to an increase in TGF-beta levels in brain and spleen cells, together with an increase in Fas and FasL mRNA expression.These results provide the evidence that the ganglioside action on the Bcl- 2, Bcl-W, Fas, and FasL expression is associated with cytokine modulation

ASSUNTO(S)

esclerose multipla encefalomielite sistema linfatico apoptose linfocinas

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