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. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: Curr Opin Microbiol. 2019 Jun 20;52:70–76. doi: 10.1016/j.mib.2019.05.005

Figure 2. Mechanisms of inflammasome activation in macrophages infected with Leishmania.

Figure 2.

NLRP3 activation requires the first signal (or priming) that can be achieved when Toll-like receptors (TLRs) ligands, TNF-α (or other cytokines) induce transcriptional upregulation of inflammasome-related genes (indicated in blue). This process usually occurs via nuclear factor-κB (NF-κB)-mediated gene expression. Leishmania is able to inhibit the inflammasome activation at the priming stage by multiple mechanisms (indicated in red). Leishmania trigger Dectin-1, a C-type lectin receptor that signals via spleen tyrosine kinase (Syk) to induce ROS, which is critical for activation of the NLRP3 inflammasome (pathway shown in green). Leishmania Lipophosphoglycan (LPG) present in the macrophage cytoplasm triggers Caspase-11 activation indirectly. This pathway feeds in the non-canonical pathway for activation of the NLRP3 inflammasome (indicated in purple).