EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - NEUTRALIZING ANTIBODY TO TGF-BETA-1 ENHANCES THE CLINICAL SEVERITY OF THE DISEASE

Experimental allergic encephalomyelitis (EAE) is a well established mo del for the human autoimmune disease multiple sclerosis. Recently, we and others have shown that the administration of TGFbeta is therapeuti cally effective in reducing incidence and severity of EAE. Here we sho w that the addition of anti-TGFbeta1 to myelin basic protein (MBP)-act ivated lymph node cells enhance the T cell proliferative response by 2 8% in vitro and in vivo and that injections of anti-TGFbeta1 antibody worsen EAE both in incidence and severity. Further, an inverse relatio nship was observed in the amount of IL-2 and TGFbeta detected in MBP s timulated culture supernatants. We show that IL-2 decreases from 248 U /ml at 48 h to non-detectable at 96 h, while TGFbeta increases from 0. 5 ng/ml to 1.2 ng/ml, respectively. These observations further indicat e a role for endogenous TGFbeta1 in the immunoregulation of EAE.