Research Interests

We seek to define the mechanisms of loss of self-tolerance and activation of autoreactive T cells in systemic autoimmune diseases and their capacity to propagate and to regulate autoreactive B cell help for pathogenic autoantibody production. In ongoing and published studies, we have demonstrated that T cells from mice with systemic autoimmune syndromes, such as lupus, are hyper-responsive to activation through their antigen receptors, compared to T cells from non-autoimmune animals, with this difference apparently an intrinsic (genetic) one. In more recent work, we have identified novel, and separable, CD4+ T cell subsets that promote autoantibody help and peripheral inflammation in lupus-prone mice. Current studies involve further characterization of these cells in mice and in humans, and dissection of the mechanisms that lead to their activation, development and aberrant effector function.