| Grant number: | 09/18227-6 |
| Support Opportunities: | Regular Research Grants |
| Start date: | August 01, 2010 |
| End date: | September 30, 2012 |
| Field of knowledge: | Health Sciences - Medicine - Medical Clinics |
| Principal Investigator: | Leonilda Maria Barbosa dos Santos |
| Grantee: | Leonilda Maria Barbosa dos Santos |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| City of the host institution: | Campinas |
Abstract
The multiple sclerosis (MS) as well as its experimental model Experimental autoimmune encephalomyelitis (EAE) are known as demyelinating diseases caused by T CD4 lymphocytes Th1 and Th17.The autoreactive T lymphocytes are generated in the periphery and migrate do the central nervous system (CNS) where they initiated the demyelination process. The autoreactive T lymphocytes produce or are stimulated by proinflammatory cytokines such as IL-17 and osteopontin.On the other hand, regulatory T cells that produced antiinflammatory cytokines such as TGFbeta and IL-10 downregulated the inflammatory process caused by the effector T cells. Cells from the innate arm of immune response such as plasmacytoid dendritic cells can either stimulated or downregulated the effect T lymphocytes. The plasmacytoid dendritic cells produce high level of indoleamine, 2,3 dioxigenase that mediated the tolerogenic function of T cells. Here, the effect of plasmacytoid dendritic cells on effector and in downregulation of autoreactive T cells will be studied either in MS patients or in the animal model (EAE). The antibody to aquaporin 4 in the serum and CSF of patients with NMO and MS. (AU)
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