Autoimmunity of Pemphigus
Similar to other autoimmune diseases, skin autoimmune diseases can be mediated by either B cells (autoantibodies) or T cells.
My lab mainly focuses on studying the autoantibody development in autoimmune skin diseases. These diseases include skin blistering diseases such as Pemphigus Vulgaris (PV), Pemphigus Foliaceus (PF), and Bullous Pemphigoid (BP), which are caused by autoantibodies against keratinocyte cell adhesion molecules. By studying the genetics of these autoantibodies, we can dissect whether their development is antigen-selected or due to non-specific activation of antibody-producing B cells (global break of tolerance).
Just as B cell-mediated autoimmune diseases require T cell help, B cells may also play a role in T cell-mediated autoimmune skin disease as B cells are also antigen presenting cells. The specificity of those disease-associated B cells may also help to determine the antigen (either self or environmental) identities which in turn may reveal the etiology of the diseases and lead to the development of novel disease treatments and/or management plans. Thus, we are also interested in understanding how B cells and antibodies participate in these T cell-mediated autoimmune diseases.
How environmental antigens may trigger the development of autoimmune diseases
We have identified an environmental antigen (one of the sand fly salivary gland antigens) that may be involved in triggering the development of an endemic skin disease. IgE antibodies against this environmental antigen may herald the onset of this disease. IgE is one of the hallmarks of allergic responses to environmental antigens (allergens). Allergy and autoimmunity are two outcomes of a dysfunctional immune system. While allergy and autoimmunity are thought to arise from maladaptive reactions against foreign and self-antigens, respectively, our studies suggest that autoantibodies may actually evolve from preceding environmental antigen-specific immune responses. Therefore, we are interested in identifying the environmental antigens or allergens that may trigger the development of autoreactive antibodies and their associated autoimmune diseases.