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. Author manuscript; available in PMC: 2014 Jul 14.
Published in final edited form as: Nat Rev Immunol. 2009 May;9(5):313–323. doi: 10.1038/nri2515

Figure 1. Model for Bacteroides fragilis-mediated protection from disease induced by Helicobacter hepaticus.

Figure 1

B. fragilis produces an immunomodulatory polysaccharide (PSA) that induces an immunoregulatory programme that provides protection from inflammation induced by H. hepaticus. PSA is taken up by intestinal dendritic cells (DCs), which presumably migrate to the local mesenteric lymph nodes (MLNs) where they initiate T-cell responses by presenting PSA on MHC class II molecules to CD4+ T cells. This process helps to restore a balanced T helper (TH) and regulatory T (TReg) cell profile. Subsequently, naive TH cells adopt anti-inflammatory functions that include expression of interleukin-10 (IL-10). IL-10 is required to suppress the production of pro-inflammatory cytokines (such as IL-17, IL-23 and tumour-necrosis factor (TNF) induced by H. hepaticus during experimental colitis. It is this balance of the pro-inflammatory responses to H. hepaticus by regulation induced by B. fragilis that results in the control of intestinal inflammation.