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. 2023 Jan 9;13:1044673. doi: 10.3389/fendo.2022.1044673

Figure 1.

Figure 1

Interactions between gut microbiota and immune system: (1). Bacteria and its derived products activate gut epithelial and immune cells to enhance gut permeability which causes the migration of microbes into submucosa. These microbes are presented by dendritic cells to T cells which polarize into Th1 and Th17 cells. Gut colonization by SFB causes the induction of Th17 cells and P. copri and L. salivarius enhances the Th1 responses. These antigen-specific Th cells activate B cells to produce IgA-ACPA. Bacteria and its products directly activate macrophages and other innate immune cells such as ILC3 or MAIT cells which lead to gut inflammation locally and further activation of T cells. (2). The interactions between fungi mainly C. albicans and phagocytes leads to induction of increased Th17 responses and decreased Treg cells which contribute to local and systemic inflammation. (3). Viral dysbiosis causes induction of Th1 responses. Upon dysbiosis in RA, these innate and adaptive immune cells migrate to joints, exaggerating inflammation. RA, rheumatoid arthritis; Th, T-helper cells, ILC3, group 3 innate lymphoid cells; MAIT, mucosa associated invariant T cells; ACPA, anti-citrullinated peptide antibodies; SFB, segmented filamentous bacteria, P.copri, Prevotella copri; L. salivarius, Lactobacillus salivarius; C.albicans, Candida albicans.