A Master Role of Symmetric Arginine Dimethylation in Lupus Autoantibody Response

Systemic lupus erythematosus is the result of the loss of immune tolerance to misguided recognitions and autoantibody production against a large number of “self” antigens. This study investigates a causal disease model in which the “self-proteins” of a major class of lupus antigens are chemically modified and subsequently become misrecognized by our own immune cells as “non-self”. We will use molecular tools of mass spectrometry and protein arrays to dissect the antigen determinants in a form of chemical modification that incites autoimmune responses.