Intestinal barrier: A gentlemen’s agreement between microbiota and immunity

Figure 2 Complex interaction between microbiota, dendritic cells and macrophages. A: CD11c⁺MHCII⁺D103⁺CX₃CR1 cells migrate to the mesenteric lymph nodes (MLN) through a C-C chemokine receptor type 7 (CCR7) dependent mechanism. These dendritic cells (DCs) can generate and activate CD8⁺ T cells and Treg Foxp3⁺ cells. These DCs also have the ability to produce transforming growth factor-β (TGF-β) and retinoic acid (RA). CD103⁺CX₃CR1^-CD11b⁺ DCs can produce interleukin (IL)-23 in response to flagellin. Other DCs in lamina propria are CD103^-CX₃CR1^intCD11b⁺; B: CD11b⁺CX₃CR1^hiCD64⁺ macrophages in the lamina propria contribute to the intestinal homeostasis through the production of anti-inflammatory cytokines and are able to recognize commensal microbiota beyond the epithelial barrier. These macrophages had previously been described as non-migratory were able to migrate into the MLNs, in a CCR7-dependent manner, carrying non-invasive bacteria captured in the intestinal lumen induces T lymphocyte responses; C: Under steady state, Th17 cells are usually found in the lamina propria of the small intestine, where its development depends on the presence of dietary antigens and commensal microbiota. These cells have important effects on the intestinal epithelium, improving the barrier function by stimulating mucin production, function of tight junction proteins, and increasing the transport of IgA to lumen. Candida albicans and Staphylococcus aureus induce Th17 cells, which produce interferon (IFN)-γ and IL-10. In the absence of microbiota, Th17 cells are not found. IL-1β, induced by commensal bacteria, is critical for differentiation of Th17 cells in the intestine.