Both toll-like receptors and nucleotide-binding oligomerization domain (NOD)-like receptors induce an inflammatory response at risk of causing tissue damage. However, the cross-regulation between interleukin-1 (IL-1) receptors and NOD2 is not completely understood. The authors show that IL-1α/β increase NOD2-induced inflammatory response by enhancing muramyl dipeptide-induced activation of MAPK signaling pathways via ERK, JNK, and P38.
- Sushan Li
- Ping Deng
- Jinyue Hu
