Figure 2.

A proposed model of the adaptive immune response in acne. The innate immune response stimulates skin cells, such as sebocytes, to secrete CXCL8, which in turn recruits CD4⁺ naïve T cells to the sites surrounding the pilosebaceous unit. CD4⁺ naïve T cells in this region receive various stimulating signals, including cytokine signals from sebocytes, pathogen stress signals from C. acnes and major histocompatibility complex signals from C. ances and seboctes-stimulated antigen presenting cells (APCs). These signals determine the differentiation of CD4⁺ naïve T cells into Th1, Th17 or Tregs. C. acnes directly induces the differentiation of CD4⁺ naïve T cells into both Th1 and Th17 cells. Th17-related cytokines secreted by sebocytes, including IL-6, TGF-β and IL-1β, as well as the IL-23 secreted by currently unidentified cells, induce the differentiation of CD4⁺ naïve T cells toward Th17. Additionally, the functional interaction between sebocytes and C. acnes induces the maturation of APCs, resulting in a preferential generation of Th17 cells over Th1 cells. The activation of Th1 and Th17 cells enhances both the innate and adaptive immune responses, while activated Tregs function as suppressors that negatively regulate the immune response.