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Candida albicans  is a fungus that is an opportunistic pathogen of humans. Normally,  C. albicans  exists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage to  C. albicans . IL-34 is a recently discovered cytokine, constitutively expressed by keratinocytes in the skin. IL-34 binds to the receptor of M-CSF, thereby stimulating tissue macrophage maturation and differentiation. Resident macrophages exhibit phenotypic plasticity and may transform into inflammatory M1 macrophages for immunity or anti-inflammatory M2 macrophages for tissue repair. M1 macrophages produce higher levels of inflammatory cytokines such as TNF α  in response to  C. albicans  stimulation. In this study, it was demonstrated that IL-34 attenuated TNF α  production by M1 macrophages challenged with heat killed Candida (HKC). The molecular mechanism of IL-34 mediated suppression of HKC induced TNF α  production by M1 macrophages was by the inhibition of M1 macrophage expression of key  C. albicans  pattern recognition receptors (PPRs), namely, Toll-like receptor (TLR) 2 and Dectin-1. The results of this study indicated that constitutive IL-34 expressed by skin keratinocytes might suppress resident macrophage responses to  C. albicans  colonisation by maintaining low levels TLR2 and Dectin-1 expression by macrophages.

IL-34 SuppressesCandida albicansInduced TNFαProduction in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2