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My research
Immunopathogenesis of vitiligo
Vitiligo vulgaris is an acquired disorder characterized by expanding depigmenting lesions of the skin, due to the disappearance of melanocytes. Several hypotheses exist for the pathogenesis of vitiligo, such as genetic predisposition, neuralchemical factors, toxic metabolites interfering with melanin metabolism, autoimmunity against melanocytes or a combination of these factors.
Accumulating evidence supports the autoimmune hypothesis, such as the presence of activated T cells and autoantibodies against melanocyte antigens in vitiligo patients. The association of vitiligo with other autoimmune diseases suggests that vitiligo is associated with decreased regulation of the immune system. We and others found that activated T cells that specifically recognize antigens on melanocytes infiltrate in the perilesional vitiligo skin. We are currently investigating how these T cells kill melanocytes in the skin leading to depigmentation. Treatments
Treatment options for vitiligo patients are UVB radiation and/or autologous skin minigrafting, which are currently available at the Netherlands Institute for Pigment Disorders of the AMC. UVB is known to suppress the immune system in the skin. We are currently investigating how this immuno-suppression leads to repigmentation of the vitiligo skin. Vitiligo development in melanoma patients has been associated with an improved prognosis. In these patients, expanded T cells that recognized melanocyte antigens expressed on both melanocytes and melanoma cells were found in the circulation and in vitiligo lesions. Melanoma
Vitiligo development has frequently been observed in immunotherapy of melanoma, suggesting that the anti-melanoma immune response also attacked normal melanocytes. Immunotherapy of melanoma is, however, hampered by the state of tolerance of the immune system towards the self-antigens on melanocytes and melanoma cells. Our research focuses on the pathogenesis of vitiligo to gain a better understanding of how tolerance to melanocyte antigens is broken in vitiligo. This research will contribute to the development of novel and innovative preventive and/or intervention strategies for vitiligo and melanoma.
My research group
Jasper van den Boorn, PhD student
Debby Konijnenberg, technician
Esther Tjin, postdoc
Daisy Picavet, technician
Wendy Dontje, postdoc Marije Kroon, MD/PhD student
Hansje-Eva Teulings, MD/PhD student
Gabrielle Krebbers, technician
This research is performed at The Netherlands Institute for Pigment Disorders (Head: Dr. J.P.W. van der Veen, MD, PhD) and the department of Dermatology (Head: Prof. dr. J.D. Bos, MD, PhD) in collaboration with Prof. dr. C.J. Melief, MD, PhD (Leiden University Medical Center) and dr. K.A Reedquist (Department of Reumatology AMC)
. Ontwerp en realisatie: Nico van Dijk Media
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