Tumour necrosis factor (p55) receptor (tnfp55r) is not essential for a cd8+ t cell mediated inflammatory response

Abstract

TNFα is a potent pro- inflammatory cytokine which mediates its responses through the binding to its specific cell surface receptors, p55 and p75. The objective of these studies is to determine the contribution of TNFpSSR in mediating the inflammatory response leading to autoimmune disease development. To assess its role in vivo, transgenic mice (RIP-gp) expressing lymphocytic choriomeningitis virus glycoprotein (LCMV-gp) in the beta islets of the pancreas (which develop diabetes after LCMV infection) were bred to mutant mice lacking the TNFp55R. Following viral infection, mice lacking TNFp55R developed hyperglycemia similar to control mice. Histologicai examination of the beta islets confirmed comparable CD8+ infiltration patterns and tissue destruction in all mice. Thus, these results demonstrate that the TNFp55R was not an essential mediator for the autoimmune response in this experimental model. These results contrast those obtained in other animal models where interference with the TNFa response prevented disease onset. Possible explanations for these findings include cytokine redundancy (IL-1) or a role for the p75 receptor in the inflammatory response.