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. 2019 May 20;10:1094. doi: 10.3389/fimmu.2019.01094

Figure 4.

Figure 4

Dysregulation of intestinal epithelial cell RIPK pathways promotes cell death in IBD. Dysregulation of RIPK (receptor interacting protein kinase) pathways play a key role in the inflammatory processes occurring in IBD (inflammatory bowel disease). TNF (tumor necrosis factor) has pleyotropic roles in intestinal epithelial cells. In homeostasis, TNF through the activation of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway, where RIPK1 has a scaffold function, it promotes cell proliferation, migration and survival, helping to a proper intestinal barrier regeneration. In IBD, TNF can induce apoptosis or necroptosis in a kinase dependent function of RIPK1 and RIPK1/3 respectively. Cell-to-cell adhesions are also loosened in IBD, allowing the translocation of food antigens and bacteria from the gut lumen. Another feature of IBD is microbial dysbiosis. Genetic mutations in RIPK2, NOD2 (nucleotide-binding oligomerization domain-containing protein 2) or ATG16L1 (autophagy-related protein 16 like 1) can impair a proper autophagy response allowing the proliferation and invasion of the host by pathogenic bacteria.