Astrocytes in multiple sclerosis

Multiple sclerosis (MS) is the commonest chronic inflammatory disorder of the central nervous system (CNS), affecting more than 1.5 million young adults worldwide. People in the prime of their working and family life suddenly face a completely different future perspective in which they become increasingly disabled. Despite intensive research, the cause and a cure of MS have remained elusive and many aspects of the pathogenesis are still not understood. The first part of this thesis deals with the current understanding on the pathophysiology of MS. The existing theories fail to explain many aspects of the disease. A major unresolved question is how anti-myelin T-cells cause lesions in the central nervous system. Anti-myelin T-cells exist in all individuals. Why cause these anti-myelin T-cells MS in only a very small fraction of the population? Previous immunohistochemical studies in our laboratory have shown that astrocytes in MS lack P2-adrenergic receptors. As P2-adrenergic receptors contribute to the suppression of inducible MHC class I1 molecules on astrocytes, their absence may play a pivotal role in inducing and perpetuating the autoimmune response in MS. This thesis further explored the role of astrocytes in the pathogenesis of MS.