Experimental allergic encephalomyelitis: neutralizing antibody to TGF beta 1 enhances the clinical severity of the disease.

Experimental allergic encephalomyelitis (EAE) is a well established model for the human autoimmune disease multiple sclerosis. Recently, we and others have shown that the administration of TGF beta is therapeutically effective in reducing incidence and severity of EAE. Here we show that the addition of anti-TGF beta 1 to myelin basic protein (MBP)-activated lymph node cells enhance the T cell proliferative response by 28% in vitro and in vivo and that injections of anti-TGF beta 1 antibody worsen EAE both in incidence and severity. Further, an inverse relationship was observed in the amount of IL-2 and TGF beta detected in MBP stimulated culture supernatants. We show that IL-2 decreases from 248 U/ml at 48 h to non-detectable at 96 h, while TGF beta increases from 0.5 ng/ml to 1.2 ng/ml, respectively. These observations further indicate a role for endogenous TGF beta 1 in the immunoregulation of EAE.