EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - INHIBITION OF CLINICAL SIGNS AND PARADOXICAL ENHANCEMENT OF LESIONS IN 2ND ATTACKS

Abstract

Experimental allergic encephalomyelitis (EAE) was induced in rats by immunization with neural antigens with or without adjuvants. A 2nd attack was induced after an interval of 3-24 wk. When the 2nd attack was produced by moderately intense active immunization or by passive tranfer, the rats were protected from clinical signs. Paradoxically, the 2nd attack regularly produced more lesions in the cerebellum than in naive controls. Inhibition of clinical sgns and the accompanying paradoxical enhancement of cerebellar lesions were independent of the type of antigen or adjuvant used for either attack, the severity of the attacks, and the time interval between them. Non-specific adrenal-mediated stress did not play any role in these phenomena. Even in the absence of clinical signs, the 2nd attack produced many lesions in the spinal cord, but these were sometimes less severe than those produced in naive controls. The observation that an initial attack of EAE had different influences on susceptibility to a 2nd attack in different parts of the nervous system is more readily explained by local tissue factors than by systemic regulatory influences.