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. 2017 Dec 22;8:1864. doi: 10.3389/fimmu.2017.01864

Figure 2.

Figure 2

Macrophage reprogramming by helminth-induced type 2 responses. Helminth-induced type 2 responses can act on macrophages on different levels, thereby impeding antimicrobial responses toward Mycobacterium tuberculosis (MTB): (A) high levels of IL-4/IL-13 downregulate C-type lectin receptor (CLR) expression in a Stat6-dependent manner, which may lead to reduced amounts of pro-inflammatory cytokines like IL-6, IL-1, or G-CSF, impaired phagocytosis and Th1/Th17 differentiation. (B) Simultaneously, IL-4/IL-13 signaling through Stat6 strongly induces Arginase1 (Arg1), which counteracts Nos2 through substrate depletion, leading to reduced NO production and less effective killing of MTB inside the phagolysosome. (C) The anti-inflammatory cytokine IL-10, produced during helminth infection, can delay phagosomal maturation. Moreover, IL10R signaling through STAT3 inhibits IL-1, IL-12, or IL-6 expression, which in turn inhibits Th1 differentiation.