| Literature DB >> 33924897 |
Astri Dewayani1,2, Kartika Afrida Fauzia3,4,5, Ricky Indra Alfaray3,4, Langgeng Agung Waskito3, Dalla Doohan3, Yudith Annisa Ayu Rezkitha6, Abdurachman Abdurachman2, Takashi Kobayashi1, Reny I'tishom7, Yoshio Yamaoka4,8,9,10, Muhammad Miftahussurur3,8.
Abstract
Although millions of people have been infected by Helicobacter pylori (H. pylori), only a small proportion of infected individuals will develop adverse outcomes, ranging from chronic gastritis to gastric cancer. Advanced development of the disease has been well-linked with chronic inflammation, which is significantly impacted by the adaptive and humoral immunity response. From the perspective of cellular immunity, this review aims to clarify the intricate axis between IL-17, IL-21, and IL-23 in H. pylori-related diseases and the pathogenesis of inflammatory gastrointestinal diseases. CD4+ helper T (Th)-17 cells, with the hallmark pleiotropic cytokine IL-17, can affect antimicrobial activity and the pathogenic immune response in the gut environment. These circumstances cannot be separated, as the existence of affiliated cytokines, including IL-21 and IL-23, help maintain Th17 and accommodate humoral immune cells. Comprehensive understanding of the dynamic interaction between molecular host responses in H. pylori-related diseases and the inflammation process may facilitate further development of immune-based therapy.Entities:
Keywords: CD4 T cell; Helicobacter pylori; T helper-17; adaptive immunity; cancer; gastrointestinal; inflammation
Year: 2021 PMID: 33924897 DOI: 10.3390/toxins13050315
Source DB: PubMed Journal: Toxins (Basel) ISSN: 2072-6651 Impact factor: 4.546