Figure 2.

The function of intestinal macrophages (MΦ) and dendritic cells (DCs) in the steady state and during inflammation/injury. In the steady state, resident CX3CR1⁺ macrophages and CD103⁺ DCs maintain tolerance toward the intestinal microbiota via the production of retinoic acid and IL-10, which, in combination with transforming growth factor (TGF)-β, induce regulatory T cells (Treg) cells. On encountering certain bacteria, CD103⁺ DCs can also produce IL-6 and IL-23, which drive type 17 helper T-cell (Th17) differentiation in a TGF-β–dependent manner. During inflammation/injury, Ly6C⁺CCR2⁺ monocytes are recruited into the intestine, where they, along with resident DCs, react to translocating bacteria through innate signaling pathways [eg, Toll-like receptor (TLR)]. These signals drive proinflammatory cytokine production, including IL-1β, tumor necrosis factor (TNF), IL-12, and IL-23, which can promote pathogenic Th1 and Th17 responses.