Fig. 3From: Cellular Toxicity and Immunological Effects of Carbon-based NanomaterialsMyD88 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-1βBack to article page