Research ArticleVitiligo

CXCL10 Is Critical for the Progression and Maintenance of Depigmentation in a Mouse Model of Vitiligo

Science Translational Medicine  12 Feb 2014:
Vol. 6, Issue 223, pp. 223ra23
DOI: 10.1126/scitranslmed.3007811

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New Skin in the Game of Vitiligo Therapy

The immune system is tasked with protecting the body from invading pathogens. Yet, sometimes, immune cells themselves attack the tissues they are supposed to protect. One such autoimmune disease is vitiligo, where immune cells are thought to attack melanocytes—the pigment-producing cells in the skin. Individuals with vitiligo have depigmented areas in their skin, which is disfiguring and also increases the risk of skin damage. Now, Rashighi et al. suggest that blocking the chemokine CXCL10 may restore pigmentation in patients with vitiligo.

The authors examined gene expression in lesional skin from vitiligo patients and found an interferon-γ–specific signature, including differential expression of the chemokine CXCL10. They found that CXCL10 was up-regulated in vitiligo patients; its receptor CXCR3 was up-regulated in T cells from these patients as well. The authors then looked in a mouse model of vitiligo to determine the functional relevance of this observation. Mice with CXCR3-deficient T cells developed a much less severe form of vitiligo, as did mice lacking CXCL10 or treated with a CXCL10-neutralizing antibody. What’s more, this CXCL10-neutralizing antibody resulted in repigmentation in mice with already established vitiligo lesions. These data suggest that CXCL10 neutralization should be considered as a potential treatment for vitiligo.