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Is MC1 dispensable for regulation of cutaneous inflammatory and immune responses?

The melanocortin‐1 receptor (MC1) – being most abundantly expressed in the skin by melanocytes – has a physiological role for melanin pigmentation in many vertebrate species. MC1 has also been implicated in regulation of skin inflammation as this receptor is detectable in the majority of non‐melanocytic cell types and its ligand α‐melanocyte‐stimulating hormone (α‐MSH) exerts immunoregulatory and anti‐inflammatory effects. However, in vivo studies on mice with targeted disruption of MC1 have been missing in the context of skin inflammation until recently. Wolnicka‐Glubisz et al. now reported that the course of ultraviolet (UV)‐induced inflammation, contact hypersensitivity, neonatal immune tolerance and UV‐induced immunosuppression is similar in MC1 signal‐deficient (C57BL/6‐Mc1re/e) and wild‐type mice. These unexpected findings are supported by own observations in experimentally induced immune‐complex‐mediated vasculitis: Mc1re/e mice exhibited a similar extent of the reverse passive cutaneous Arthus reaction compared with wild‐type animals. Future studies are thus needed to clarify whether these findings are due to limitations in the chosen mouse model and/or point to additional MC subtypes that may regulate inflammatory and immune responses in the skin.