Role of Tob1 - a member of the anti-proliferative (APRO) family - in experimental autoimmune encephalomyelitis and motor neuron dysfunction
Final Report Abstract
Together with previous observations in the lab, my results provide direct evidence that B cells can have an essential role in vivo independent of Ig secretion to the pathogenesis of EAE. In human MOG protein-induced EAE, I demonstrated that activated MOG-reactive B cells are capable of efficiently presenting MOG protein and promoting differentiation of pathogenic MOG-specific T cells, which results in acute CNS inflammation. The results further indicate that independently of MOG-specific antibody secretion, myelin-reactive B cells are sufficient to induce spontaneous EAE in MOG-TCR Tg mice. Furthermore, the results argue for a minor role of Ag-transfer via BCR in rhMOG induced EAE. Generation and characterization of bm chimera mice containing MHC II-deficient MOG-specific B cells has been already performed. Due to delays in breeding I anticipate finishing bm studies using MHC II-deficient NP-specific B-cells. I will also focus on the characterization of T cell responses in bm chimeras containing MOG-specific or NP-specific MHC II-deficient or -sufficient B cells.
