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. 2019 Apr 11;16:18. doi: 10.1186/s12989-019-0299-z

Fig. 3.

Fig. 3

MyD88 played a critical role in alveolar macrophage-mediated inflammatory response to CNTs. MyD88 mediated CNTs toxicity by linking IL-1R or TLR-dependent signaling and acted on downstream IRAKs and TRAFs, thus inducing proinflammatory NF-κB pathway. Also, MAPKs was involved in toxic response and MAPK inhibitors for p38 and JNK reduced levels of TNF-α and IL-1β. MyD88-specific inhibitory peptide blocked the production of TNF-α and IL-1β