Autoimmune diseases are the consequence of the body's failure to delete all self-reactive high affinity T cell clones during lymphocyte development. In autoimmune vitiligo, circulating T cells bearing high affinity TCRs against melanocyte specific differentiation antigens infiltrate the skin and kill melanocytes, producing patches of depigmented skin characteristic of the disease. Vitiligo's T cell mediated immune response against melanocytes is highly efficient.

Melanoma tumors have a similar antigenic repertoire as melanocytes, but melanoma-infiltrating T cells rarely induce a strong enough immune response to elicit tumor regression. The relative inability of these cells to recognize tumor cells suggests that melanoma derived T cells have low avidity and express low affinity TCRs, in addition to being immersed in an immunosuppressive environment that may explain their therapeutic ineffectiveness.

The working hypothesis is that the strong reaction seen in autoimmune vitiligo results from high avidity T cells expressing high affinity TCR; furthermore, given the antigenic similarities between melanoma cells and melanocytes, vitiligo T cells have a superior therapeutic potential than their melanoma counterparts. To test the hypothesis that vitiligo derived T cells have, on average, higher avidity than melanoma derived T cells, T cells from both diseases and will be isolated and their reactivity compared. TCRs from melanocyte specific differentiation antigen reactive T cells will then be cloned and their affinity measured.