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Irritant Contact Dermatitis (ICD) is characterized by epidermal hyperplasia and inflammatory cytokine release. IL-6 has been shown to be involved in the pathogenesis of ICD; however, the involvement of the IL-22/IL-22R α  axis and its relation to IL-6 in the inflammatory response following irritant exposure are unknown. Using a chemical model of ICD, it was observed that mice with a keratinocyte-specific knockout of IL-6R α  (IL-6R α  Δker ) presented with increased inflammation and IL-22R α  and IL-22 protein expression relative to WT following irritant exposure, indicating that IL-6R α  deficiency in epidermal keratinocytes leads to the upregulation of IL-22R α  and its ligand during ICD. Furthermore, it was shown that IL-6 negatively regulates the expression of IL-22R α  on epidermal keratinocytes. This effect is functional as the effects of IL-22 on keratinocyte proliferation and differentiation were markedly reduced when keratinocytes were pretreated with IL-6 prior to IL-22 treatment. These results show that IL-6 modulates the IL-22/IL-22R α  axis in the skin and suggest that this occurrence may be associated with the increased epidermal hyperplasia and exacerbated inflammatory response observed in IL-6R α  Δker  mice during ICD.

IL-6 Negatively Regulates IL-22RαExpression on Epidermal Keratinocytes: Implications for Irritant Contact Dermatitis