Current work is focused on the chronic- relapsing model experimental allergic encephalomyelitis (EAE). This disease is produced by transfer lymphocytes sensitized to myelin basic protein (MBP) or proteolipid protein to syngeneic mice. Neurologic dysfunction is characterized pathologically by inflammation and primary demyelination. The immunological mechanisms responsible for the initial episode and for the chronic disease are being investigated. Particular attention has focused on the role of activated T cells and regulatory mechanism occurring at the level of EAE lesion. Previous studies have demonstrated that transforming growth factor beta (TGF-beta 1) can reduce the clinical severity of EAE even when given after the initial onset of disease. Recent studies have demonstrated that the administration of soluble MBP, given the following cell transfer or even after the onset of clinical disease, can also ameliorate clinical illness. It is thought that the mechanism for this effect is the induction of apoptosis or programmed cell death. T cells which are activated and encountered antigen go without a second signal i.e., IL-2 may be induced to undergo apoptosis. Finally, the role of superantigens such as staphylococcal enterotoxin B have been shown to produce sufficient activation of T cells previously sensitized to MBP to allow transfer of disease. These findings indicate nonspecific activation factors could contribute to autoimmune disease process.
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