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.
 

Photo courtesy of Dr. Vincent Liu
 
Cutaneous T cell lymphomas (CTCLs) are hematopoietic malignancies derived from skin-homing CD4 T cells and have been increasing in incidence over the last 30 years.  This group of diseases include localized malignancies that are restricted to small patches of skin, which carry a favorable prognosis, as well as leukemic forms of the disease, including Sézary syndrome, that exhibit malignant circulating cells.  Despite a growing number of targeted therapies in lymphoma becoming available and being assessed for efficacy in CTCL and Sézary syndrome, there are currently no validated biomarkers that can be used to predict treatment response or guide therapeutic choice.  Efficacy of systemic treatments in leukemic CTCL and Sézary syndrome remains poor; these forms of the disease are often refractory to multiple, serial treatments and carry a five year median survival of less than 20%.  Our efforts in the lab are to identify the genetic and molecular perturbations among the different forms of CTCL in order to better match patients with the treatment course that will be most effective.