Immune Responses Mediated by Th17 Cells in <b><i>Helicobacter pylori </i></b>Infection

Abstract

T helper 17 (Th17) cells are one of the CD4+ T-cell subsets which induce a variety of diseases by secreting IL-17 and other inflammatory factors. After Helicobacter pylori (Hp) infection, cytotoxin-associated gene A and urease subunit B regulate the number of Th17 cells via induction of cell differentiation by infected macrophages, activation of MyD88 and other pathways, and by driving chemokines, which upregulates the number of both Th17 cells and regulatory T cells (Tregs) and switches towards a Treg-type immune response. Meanwhile, Th17 cells also play important roles in the response to Hp infection, participating in the clearance of Hp by recruiting neutrophils and expanding inflammatory response, causing mucosal damage and even inducing cancer. Thereby, Th17 cells participate in the occurrence and development of Hp-related diseases, such as gastritis, peptic ulcer disease and gastric cancer.

Immunological markers and Helicobacter pylori in patients with stomach cancer: Expression and correlation

“…The host factors which may affect the elimination or proliferation of H. pylori (44) were also analyzed in the present study. Gastric biopsies were obtained to determine the mRNA expression levels of interleukins, master transcription factors and co-modulators of the immune response.…”

The Roles of IL-17, IL-21, and IL-23 in the Helicobacter pylori Infection and Gastrointestinal Inflammation: A Review

“…The function of Th17 cells remains contradictory although they tend to display a proinflammatory function in the context of H. pylori disease. IL-17 is required to facilitate bacterial clearance, though the levels produced may be insufficient for extensive clearance and may cause IL-17-mediated-diseases from inflammation [ 71 ]. The IL-17 family could induce numerous immune regulatory and proinflammatory factors related to local tissue, such as antimicrobial peptides (b-defensin and S100 protein), chemokines (CXCL1, CXCL-5, CCL-2, CCL-20), and MMPs.…”

“…In early colonization, H. pylori modulates immature “tolerogenic” DCs that skew the Th17/Treg balance toward Treg. H. pylori -infected patients with gastritis display an inverse correlation between the Th17/Treg ratio and bacterial density, indicating Tregs may reduce inflammation and provide pathogen persistent [ 61 , 71 ]. The plasticity of Th17/Treg is demonstrated by the ability of Treg to turn into Th17 or vice versa, where co-expression of both Treg and Th17 (FOXP3 and RORγt) signature genes reside in the same cell.…”

GM‐CSF is key in the efficacy of vaccine‐induced reduction of Helicobacter pylori infection

“…Key studies have demonstrated that CD4 + Th cells confer protection against H. pylori 17–20 . In particular, Th17 cells produce a number of cytokines, such as IL‐17 and IL‐22, which are key players in the mediation of adaptive immune responses against H. pylori infection, and in the vaccine‐induced clearance of H. pylori 20–22 …”

“…[17][18][19][20] In particular, Th17 cells produce a number of cytokines, such as IL-17 and IL-22, which are key players in the mediation of adaptive immune responses against H. pylori infection, and in the vaccine-induced clearance of H. pylori. [20][21][22] IL-22, in response to H. pylori infection, triggers the production of antimicrobial peptides (AMPs) such as regenerating islet-derived protein 3-beta (RegIIIβ) by gastric epithelial cells. RegIIIβ is one of the key molecules involved in vaccine-induced reduction of H. pylori colonization in mice.…”