Alopecia areata is an autoimmune disease characterized by nonscarring hair loss that is often episodic but may progress to more severe forms that involve the entire body and last a lifetime.  While normally the hair follicle employs various mechanisms to prevent it from being the target of immune attack, this so-called “immune privileged” status appears to be disrupted in alopecia areata.  Work done on animal models and supported by examinations of involved human tissues implicate CD8 T cells as the most proximal direct effectors of disease, although the dysregulated pathways and mechanisms that lead to pathological attack of self tissues are not well described.  One of the primary focuses of the lab is identifying the immunological aberrancies that cause alopecia areata and autoimmune diseases of skin and hair in general.  We aim to elucidate the cellular and molecular mechanisms responsible for loss of immune privilege and autoimmune attack of the hair follicle in alopecia areata in order to identify novel therapeutic targets and uncover themes consistent across autoimmune diseases in humans.