Gut microbiota are known to influence mucosal immunity, but less is known about the role played by skin microbiota. In Science, Naik et al. show that skin commensals, such as Staphylococcus epidermidis, tune local T cell responses to cutaneous infection. Skin-resident T cells and innate lymphocytes produce interferon-γ and interleukin 17 (IL-17), but this ability is impaired in germ-free mice. Monocolonization of germ-free mice with gut commensals does not restore IL-17 production, but colonization with S. epidermidis rescues this ability. Unlike local gut responses that rely on IL-23 signaling, skin responses depend on production of IL-1 to elicit IL-17 by αβ and γδ T cells. IL-1R1–MyD88 signaling, but not TLR or IL-6 signaling, elicits local skin responses, counterbalanced by keratinocyte production of IL-1 receptor antagonist (IL-1RA). Thus local commensals are necessary to influence adaptive immune responses in both gut and skin environments.

Science (26 July 2012) doi:10.1126/science.1225152