Th17 Cells in Helicobacter pylori Infection: a Dichotomy of Help and Harm.
Helicobacter pylori is a Gram-negative bacterium that infects the gastric epithelia of its human host. Everyone who is colonized with these pathogenic bacteria can develop gastric inflammation, termed gastritis. Additionally, a small proportion of colonized people develop more adverse outcomes, including gastric ulcer disease, gastric adenocarcinoma, or gastric mucosa-associated lymphoid tissue lymphoma. The development of these adverse outcomes is dependent on the establishment of a chronic inflammatory response. The development and control of this chronic inflammatory response are significantly impacted by CD4+ T helper cell activity. Noteworthy, T helper 17 (Th17) cells, a proinflammatory subset of CD4+ T cells, produce several proinflammatory cytokines that activate innate immune cell antimicrobial activity, drive a pathogenic immune response, regulate B cell responses, and participate in wound healing. Therefore, this review was written to take an intricate look at the involvement of Th17 cells and their affiliated cytokines (interleukin-17A [IL-17A], IL-17F, IL-21, IL-22, and IL-26) in regulating the immune response to H. pylori colonization and carcinogenesis.
['Dixon|Beverly R E A|BREA|', 'Hossain|Rafat|R|', 'Patel|Rachna V|RV|', 'Algood|Holly M Scott|HMS|']
D016207:Cytokines D005786:Gene Expression Regulation D016481:Helicobacter Infections D016480:Helicobacter pylori D006801:Humans D058504:Th17 Cells
Th17 cells Helicobacter pylori inflammation gastritis IL-21 carcinogenesis IL-17