Mechanisms of systemic autoimmunity in murine models of SLE.

Our laboratory has utilized spontaneous and experimentally induced models of systemic autoimmunity in mice in order to elucidate the cellular deficiencies in immunoregulation that are essential to this process. In the spontaneously autoimmune mouse strains, genetic defects in T and B cell tolerance are the primary abnormalities that drive the syndrome. The induced chronic graft-vs-host model depends on abnormal T-B interactions resulting from allogeneic recognition of major histocompatibility complex (MHC) class II. Future investigations will target the biochemistry of the loss of tolerance and the specificity of autoreactive T cells that provide help for autoantibody production.