Prevention and therapy of experimental autoimmune neuritis by an antibody against T cell receptors-alpha/beta.

摘要: The mAb R73 directed to the TCR-alpha/beta of rat lymphocytes was tested for its therapeutic potential during effector phase experimental autoimmune neuritis (EAN) in Lewis rats. EAN can be actively induced by immunization with bovine peripheral nerve myelin, P2 protein, or a peptide containing neuritogenic epitope and serves as model human Guilain-Barre syndrome. Adoptive transfer activated P2-specific T also produces monophasic disease (AT-EAN) characterized inflammation demyelination nerves highlights central role pathogenesis EAN. A single administration immediately after injection line cells completely prevented development clinical electrophysiologic signs most animals greatly alleviated others. In further experiments applied appearance first myelin. both cases anti-TCR-alpha/beta reversed dysfunction. vivo vitro data suggest that impairment Ag recognition cell function occupancy TCR R73-induced TCR-modulation rather than depletion TCR-alpha/beta-bearing is decisive mechanism underlying suppression apparent already within 48 h injection.