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The role of γδ T cells in the interaction between commensal and pathogenic bacteria in the intestinal mucosa

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Pages 379-392 | Received 23 Mar 2022, Accepted 06 May 2022, Published online: 18 May 2022
 

Abstract

The intestinal mucosa is an important structure involved in resistance to pathogen infection. It is mainly composed of four barriers, which have different but interrelated functions. Pathogenic bacteria can damage these intestinal mucosal barriers. Here, we mainly review the mechanisms of pathogen damage to biological barriers. Most γδ T cells are located on the surface of the intestinal mucosa, with the ability to migrate and engage in crosstalk with microorganisms. Commensal bacteria are involved in the activation and migration of γδ T cells to monitor the invasion of pathogens. Pathogen invasion alters the migration pattern of γδ T cells. γδ T cells accelerate pathogen clearance and limit opportunistic invasion of commensal bacteria. By discussing these interactions among γδ T cells, commensal bacteria and pathogenic bacteria, we suggest that γδ T cells may link the interactions between commensal bacteria and pathogenic bacteria.

Authors’ contributions

XW conceived the concept, wrote the article and prepared figures. HY revised the manuscript. HY and BG provided the funds.

Disclosure statement

The authors report no conflict of interest.

Additional information

Funding

This research was supported by the National Natural Science Foundation of China (8210082023, 81871734, 81471994), Key R & D Program of Jiangsu Province (BE2020646), Jiangsu Provincial Medical Talent (ZDRCA2016053), Six talent peaks project of Jiangsu Province (WSN-135), Advanced health talent of six-one project of Jiangsu Province (LGY2016042), the "Peak Project" Scientific Research Special Funding (2021DFJH0008), the Xuzhou Science and Technology planning Project (KC20116), Natural Science Research Project of Higher Education Institutions in Jiangsu Province (20KJB310013) and Xuzhou Medical University Excellent Talent Introduction Project (D2019030).

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