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Infiltrating M1 macrophages polarized via either Notch/NF-B crosstalk or prostaglandin receptor EP3/Rho kinase signaling secrete pro-inflammatory cytokines that exacerbate tubular necroptosis, extracellular matrix deposition, and renal fibrosis (136, 137)

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Intestinal neuroendocrine cells and goblet cells are mediators of IL-17A-amplified epithelial IL-17C production in human inflammatory bowel disease

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