Figure 2.

Immunological pathways of against cutaneous leishmaniasis. This figure shows different immunological pathways in CL that all depend on the differentiation of CD4+ T cell subsets into Th1, Th2, Treg, and Th17. Following parasite entry, APCs (macrophages and dendritic cells) are stimulated to produce pro-inflammatory cytokines such as IL-12. These cytokines promote Th1 differentiation and IFN-γ production lead to activation of macrophages and parasite killing by NO production. Conversely, anti-inflammatory cytokines promote differentiation of Th0 toward Th2 that inhibit macrophage activity and lead to parasite survival. Overproduction of inflammatory cytokines results in severe immunopathology and non-healing infection. TGF-β and IL-27 cytokines secreted by macrophages or DCs stimulate Treg cells to produce IL-10 that act back on the macrophages and DCs to reduce the release of inflammatory mediators, forming a negative feedback loop and the balance of pro- and anti-inflammatory cytokines controls pathology and tissue destruction.