Th17 Cells and Activated Dendritic Cells Are Increased in Vitiligo Lesions

Vitiligo is a common skin disorder, characterized by progressive skin de-pigmentation due to the loss of cutaneous melanocytes. The exact cause of melanocyte loss remains unclear, but a large number of observations have pointed to the important role of cellular immunity in vitiligo pathogenesis.In this study, we characterized T cell and inflammation-related dermal dendritic cell (DC) subsets in pigmented non-lesional, leading edge and depigmented lesional vitiligo skin. By immunohistochemistry staining, we observed enhanced populations of CD11c+ myeloid dermal DCs and CD207+ Langerhans cells in leading edge vitiligo biopsies. DC-LAMP+ and CD1c+ sub-populations of dermal DCs expanded significantly in leading edge and lesional vitiligo skin. We also detected elevated tissue mRNA levels of IL-17A in leading edge skin biopsies of vitiligo patients, as well as IL-17A positive T cells by immunohistochemistry and immunofluorescence. Langerhans cells with activated inflammasomes were also noted in lesional vitiligo skin, along with increased IL-1ß mRNA, which suggest the potential of Langerhans cells to drive Th17 activation in vitiligo.These studies provided direct tissue evidence that implicates active Th17 cells in vitiligo skin lesions. We characterized new cellular immune elements, in the active margins of vitiligo lesions (e.g. populations of epidermal and dermal dendritic cells subsets), which could potentially drive the inflammatory responses

Stimulation of transplantation immunity and plasma cell reaction by interferon in mice.

It is assumed that interferon is a necessary component of the formation of immunological reactivity. At the same time interferon may serve as a factor stimulating immunity as a whole. Administration of interferon to mice, recipients of skin allografts, brings about acceleration of rejection process and stimulation of the cytotoxic activity of lymphocytes of mice towards target cells. With the repeated transplantations to mice treated with interferon in the first grafting, acceleration of rejection of new grafts (the `second set' phenomenon) is observed. Intrasplenic inoculation of interferon to mice at the time of antigen administration results in intensified plasma cell reaction in the spleens