Molecular Mechanisms of Reduced Susceptibility of ADAP-deficient Mice to Experimental Autoimmune Encephalomyelitis (EAE)

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The adhesion and degranulation-promoting adapter protein (ADAP), expressed in T cells, myeloid cells, and platelets, is known to regulate receptor-mediated inside-out signalling leading to integrin activation and adhesion. In previous studies we demonstrated that upon induction of experimental autoimmune encephalomyelitis (EAE) ADAP-deficient mice develop a significantly milder clinical course of disease and that this effect is T cell-independent. The aim of this project is to dissect the cellular and molecular mechanisms of the reduced inflammatory infiltration of the CNS and the lymphocyte accumulation in the lymph nodes of ADAP-deficient mice. For these purposes, we will analyze the impact of conditional ADAP-knockout mice on the course of EAE.