期刊
INFECTION AND IMMUNITY
卷 87, 期 11, 页码 -出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00363-19
关键词
gastritis; Helicobacter pylori; IL-17; IL-21; inflammation; Th17 cells; carcinogenesis
资金
- Office of Medical Research, Veterans Affairs Merit Review [IBX000915A]
- NIH [P30DK058404]
- Vanderbilt University Digestive Disease Research Center
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.
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