Study of the migratory, effector and regulatory pattern of plasmacytoid dendritic cells and B lymphocytes present in the central nervous system during the inflammatory process in experimental autoimmune encephalomyelitis in Lewis rats

• Grant number: 13/09085-9
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Effective date (Start): January 01, 2014
• Effective date (End): August 31, 2014
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Alessandro dos Santos Farias
• Grantee: Michelle Rocha Parise
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 11/18728-5 - Study of migratory, effector and regulatory pattern of autoreactive t lymphocytes, previously transduced with GFP in experimental demyelinating diseases, AP.JP

Abstract

Multiple Sclerosis (MS) is a chronic, inflammatory and demyelinating disease of the central nervous system. Although its etiology remains unknown, it is believed that is an autoimmune disease mediated by CD4 + T cells. The experimental autoimmune encephalomyelitis (EAE) is an experimental model of disease mediated by adoptive transfer of effector CD4 + T cells, used for studying MS. The features of this model are inflammation and demyelination, resembling the MS. The effector function of T lymphocytes may be decreased by regulating mechanisms of cells that co-migrate to the CNS. In this study, we will employ the technique of retroviral transduction of GFP to the autoreactive T cells, a technique already established in our laboratory. This method allows a permanent marking and analysis of self-reactive cells (encephalitogenic) in vitro, ex vivo and in vivo by flow cytometry and/or confocal microscopy. Our previous results showed that addition of encephalitogenic cells (GFP+) other CD4+ T lymphocytes (GFP-), as well as B lymphocytes, dendritic cells and CD8+ T cells are present in the central nervous system throughout the course of the disease. These cells can both participate in the genesis of disease as may be directly related to the control of inflammation and consequently with remission of clinical signs of EAE. Thus, we can separate the encephalitogenic cells from other cells that co-migrate to the CNS, specifically B cells and plasmacytoid dendritic cells, analyzing their function (effector and/or regulatory) during the clinical course of EAE.