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Review
. 2021 Aug;385(2):305-322.
doi: 10.1007/s00441-020-03351-1. Epub 2021 Jan 26.

Immune regulation in renal inflammation

Katrin Neumann  1   2 , Gisa Tiegs  3   4
Affiliations
Review

Immune regulation in renal inflammation

Katrin Neumann et al. Cell Tissue Res. 2021 Aug.

Abstract

Renal inflammation, induced by autoantigen recognition or toxic drugs, leads to renal tissue injury and decline in kidney function. Recent studies have demonstrated the crucial role for regulatory T cells in suppressing pathogenic adaptive but also innate immune responses in the inflamed kidney. However, there is also evidence for other immune cell populations with immunosuppressive function in renal inflammation. This review summarizes mechanisms of immune cell regulation in immune-mediated glomerulonephritis and acute and chronic nephrotoxicity.

Keywords: ILC2; Immune regulation; Immune-mediated glomerulonephritis; Nephrotoxicity; Regulatory T cells.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Mechanisms of Treg activation and depletion in immune-mediated GN. Treg activation and function is supported by IL-2, IL-10 and the IL-2/anti-IL-2 mAb complex in immune-mediated GN thereby suppressing the inflammatory Th1 and Th17 response. In contrast, Treg depletion due to IL-2 deficiency or blockage of CD25 increases Th1- and Th17-mediated immunity
Fig. 2
Fig. 2
Mechanisms of Treg activation in acute and chronic nephrotoxicity. Application of the IL-2/anti-IL-2 mAb complex as well as the cytokines IL-2, IL-33 or IL-233 induce c and expansion and protect against tissue damage in acute and chronic nephrotoxicity by inhibiting innate immune responses. N: neutrophils, M1: M1 macrophages
Fig. 3
Fig. 3
Activation and function of ILC2 in kidney disease. Application of IL-33 induces activation and expansion of renal ILC2 while IFNγ has an inhibitory effect. Activated ILC2 exert an immunosuppressive function in adriamycin nephropathy through inhibition of M1 macrophages and neutrophils as well as activation and recruitment of eosinophils. In IRI, treatment with the IL-2/anti-IL-2 mAb complex induces ILCreg, which promote M2 macrophage polarisation by production of TGFβ and IL-10. N: neutrophils, M1: M1 macrophages, Eos: eosinophils, M2: M2 macrophages
See this image and copyright information in PMC

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