The Jabbari lab studies alopecia areata (AA), an autoimmune disease of the hair follicle characterized by follicular infiltration of immune cells, comprised predominantly of CD4 and CD8 T cells. AA is estimated to affect up to 6 million people in the United States at some point during their lifetime and commonly affects patients younger than 20 years old, which can have a damaging impact on their self-esteem. The aim of the lab is to identify effector cell populations and cytokine pathways that are involved in the pathogenesis of disease utilizing the C3H/HeJ mouse model and human skin samples.
Recent work in the field has primarily focused on the contribution of CD8 T cells and has highlighted NKG2D+ CD8 T cells as pathogenic effector cells in the attack of the hair follicle. However, the involvement of CD4 T cells in the pathogenesis of disease is still not fully known. Preliminary data from the lab, as well as work from other groups, has indicated that CD4 T cells are able to induce disease when isolated from AA mice and transferred into recipient mice. Additionally, it has been well-established that IFNg is a pivotal cytokine in AA, and our lab has found that the skin draining lymph nodes of AA mice have a higher number of IFNg+CD4+ T cells, suggesting a role of CD4 derived IFNg in the pathogenesis of disease.
My project in the lab is to identify the roles that CD4 T cells and CD4 derived IFNg play on the loss of hair follicle tolerance and the development of disease.