T Cells and Acute Kidney Injury: A Two-Way Relationship

Frontiers in Immunology

Jeremy S. Leventhal¹  Paolo Cravedi²  Sergio Dellepiane² 

[1] Division of Nephrology, White Plains Hospital, White Plains, NY, United States;Icahn School of Medicine at Mount Sinai, New York, NY, United States;

关键词: AKI;    IRI;    regulatory T cell;    Treg;    TH1;    TH2;   

DOI  :  10.3389/fimmu.2020.01546

来源: DOAJ

【 摘 要 】

Acute Kidney Injury (AKI) complicates up to 10% of hospital admissions substantially increasing patient morbidity and mortality. Experimental evidence supports that AKI initiation and maintenance results from immune-mediated damage. Exogenous injury sources directly damage renal cells which produce pro-inflammatory mediators recruiting immune cells and furthering kidney injury. Many AKI studies focus on activation of innate immunity; major components include complement pathways, neutrophils, and monocytes. Recently, growing evidence emphasizes T lymphocytes role in affecting AKI pathogenesis and magnitude. In particular, T helper 17 lymphocytes enhance tissue injury by recruiting neutrophils and other inflammatory cells, while regulatory T cells conversely reduce renal injury and facilitate repair. Intriguingly, evidence supports local parenchymal-T cell interactions as essential to producing T cell phenotypic changes affecting long-term kidney and patient survival. Herein, we review T cells effects on AKI and patient outcomes and discuss related new therapeutic approaches to improve outcomes of affected individuals.

【 授权许可】

Unknown