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. 2013 Oct 3;140(3):323–334. doi: 10.1111/imm.12140

Figure 7.

Figure 7

Schematic diagram representing anti-mycobacterial mechanism of interleukin-17A (IL-17A). In response to bacillus Calmette–Guérin (BCG) infection, activated macrophages express of inducible nitric oxide synthase (iNOS) and produce nitric oxide (NO). We propose that IL-17A enhances BCG-induced phosphorylation of Jun N-terminal kinase (JNK), which in turn up-regulates the expression of iNOS and hence production of NO. Enhanced NO production eventually facilitates the clearance of intracellular survival of BCG.