Experimental allergic encephalomyelitis: Neutralizing antibody to TGFβ1 enhances the clinical severity of the disease

Abstract

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 TGFβ is therapeutically effective in reducing incidence and severity of EAE. Here we show that the addition of anti-TGFβ1 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-TGFβ1 antibody worsen EAE both in incidence and severity. Further, an inverse relationship was observed in the amount of IL-2 and TGFβ 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 TGFβ increases from 0.5 ng/ml to 1.2 ng/ml, respectively. These observations further indicate a role for endogenous TGFβ1 in the immunoregulation of EAE.