Research interests: Mechanisms underlying sex-related differences in autoimmune disease; meningeal inflammation and how it impacts CNS degenerative disease. Multiple Sclerosis, a CNS inflammatory disease, is the result of dysregulation of normally protective immune responses. In this disease, pathogenic immune cells gain access to the brain and spinal cord and the ensuing inflammation causes damage to myelinated nerves. Our laboratory studies how certain classes of innate immune cells, particularly mast cells and innate lymphoid cells, promote Multiple Sclerosis (MS), a CNS demyelinating disease, regulate these aberrant responses. Using a rodent model of MS, Experimental autoimmune/allergic encephalomyelitis (EAE), our work has shown that mast cells in the meninges are activated early in this disease and promote the opening of the blood brain barrier (BBB), vasculature that is relatively impermeable and normally sequesters the CNS from the entry of inflammatory cells. Current studies are focused on understanding how meningeal mast cells influence these events. In the process, we have established a new paradigm for the mast cell mediated inflammation of the meninges in immunity. A second line of research investigates the basis for sex-determined differences in MS. It is well established that females show a 3:1 higher incidence and distinct disease presentation than men. Using a mouse model of disease that recapitulates this sex dimorphism in susceptibility, we are studying the role of hormones in altering the immune responses that exacerbate disease in females and protect from disease in males.