Research Paper Volume 12, Issue 17 pp 17528—17540
Two identified subsets of CD8 T cells in obstructed kidneys play different roles in inflammation and fibrosis
- 1 College of Veterinary Medicine, China Agricultural University, Beijing 100193, China
- 2 Department of Nephrology, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai 200080, China
- 3 Animal Husbandry and Veterinary Department, Beijing Vocational College of Agriculture, Beijing 102442, China
Received: April 10, 2020 Accepted: July 7, 2020 Published: September 13, 2020https://doi.org/10.18632/aging.103764
How to Cite
Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Inflammation plays a crucial role in initiating renal fibrosis after injury. The infiltration of inflammatory cells, such as CD4+ T cells and macrophages, contributes to renal fibrosis following ureteric obstruction. However, the function of CD8+ T cells in obstructed kidneys remains unclear. Although CD8+ T cell depletion intensifies renal fibrosis by decreasing IFN-γ and increasing IL-4 in the kidneys, the change and role of CD8 T cell populations following environmental changes during renal fibrosis are largely unknown. Here, we identified two CD8 T cell subsets in mouse obstructed kidneys with unilateral ureteric obstruction and revealed their different functions in building an inflammatory or profibrotic environment. Following renal fibrosis, the phenotypes of infiltrated CD8 T cells were mainly Tc1 (CD44+CD25−CD62L−) at the early inflammation stage and then changed to Tc2 (CD44+CD25highCD62Llow). Tc1 and Tc2 secreted IFN-γ, contributing to the decrease in the Th2-induced over-polarization of M2 macrophages and fibrosis. Moreover, Tc2 secreted pro- and anti-inflammation factors and decreased the inflammatory responses of other cells to control inflammation and fibrosis. This work and our previous study showed that CD8 T cells could balance out inflammation by controlling its level in renal fibrosis.