| abstract |
The present invention is related to the development and treatment of autoimmune disease. Autoimmune diseases can result from tissue damage caused by the activation of autoreactive T cells by autoantigens. For example, peptide fragments of naturally occurring proteins (i.e., for example, chromogranin A) may activate autoreactive T cells that result in the destruction of pancreatic β islet cells, possibly by the release of inflammatory cytokines (i.e., for example, interferon-γ). One naturally occurring biologically active chromogranin A peptide fragment, WE14, may comprise a diabetogenic autoantigen. Truncation and extension analysis of WE14 indicates that the stimulating binding register of WE14 occupies only half of the mouse IA g7 peptide binding groove, leaving positions p1 to p4 empty. Inhibition of autoantigen-autoreactive T cell binding may provide therapeutic as well a prophylactic treatments for autoimmune diseases |