Fig. 2
From: Triggers for the onset and recurrence of psoriasis: a review and update
Potential role of infections and dysbiosis of skin microbiota in triggering psoriasis (by Figdraw, www.figdraw.com). Streptococcal tonsillitis may trigger psoriasis through various mechanisms: a) M protein of Streptococcus pyogenes (S.P.) mimicking human K17, b) superantigens of S.P. activating the release of IL-12 and then promoting the expression of skin-homing CLA in CD4 + T cells, and c) adjuvant effects of streptococcal PG. Regarding to other infections, macrophages (Møs) presents PG of Staphylococcus aureus (S.A.) and S.P. by HLA-DR to CD4 + T cells, leading to the proliferation of CD4 + T and the production of IFN-γ. S.P and Candida albicans (C.A.) colonizing in psoriatic lesions induce the migration of IL-17–producing CLA + T cells to the skin and expression of psoriasis autoantigens like ADAMTSL5, which is recognized by autoreactive CD8 + T cells in epidermis. The C. A. infection also induces IL-17 production by CD4 + TRM. Virus infection activates RIG-I antiviral signaling in CD11c + DCs and induces the IL-23 expression through NF-κB. A vicious cycle starting from barrier destruction to microbiota disturbance, then to lesion aggravation promotes the formation of psoriatic inflammation. The high level of Corynebacterium in psoriatic skin lesions induces an intense IL-17 and IL-23-dependent response of γδT17