This finding is in agreement with clinical studies suggesting that MN‐derived TNF‐α and IL‐1β are high‐level drivers of intestinal inflammation in IBD.[110, 111] We showed that iDCs properly matured, underwent activation, and exhibited apical antigen sampling functions, as inflammatory stimuli induced higher levels of GM‐CSF in IEB model‐iDC co‐cultures (Figure 6b‐iii). Here, CSF2 is linked to inflammatory bowel disease.