Another area of active investigation in the lab concentrates on weakened muscle conditions known as inflammatory myopathies. This group of autoimmune diseases is marked by chronic inflammation of muscle tissue. These inflammatory myopathies are part of a heterogeneous group of diseases with diverse etiologies and clinical manifestations. Importantly, the cause of these diseases remains unclear and could hold the key to understanding the pathogenic mechanisms of autoreactive lymphocyte activation, expansion, and myositic inflammation.
Our work in this area examines the role of Tregs in the development of muscle tissue inflammation through the use and development of novel animal models of these diseases. Specifically, we are examining the interplay between genetics and the environment in promoting an abnormal display of antigens that, in the absence of normal Treg function, allows for the development of myositis. The active role of Tregs in suppressing the inflammatory response of autoreactive cells primed through endogenous antigen exposure has been clearly established in our laboratory. In December 2013, we published Aberrant muscle antigen exposure in mice is sufficient to cause myositis in a Treg cell-deficient milieu
and were reviewed here