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New insights into immune cell diversity in acute kidney injury

Cellular & Molecular Immunology volume 20, pages 680–682 (2023)Cite this article

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Acute kidney injury (AKI) is a frequent complication affecting hospitalized patients in medical wards and usually arises from ischemia‒reperfusion injury (IRI), sepsis, and nephrotoxic drugs. Excess infiltration and activation of immune cells in the kidney induce a continuous inflammatory response, which is characterized by substantial cytotoxicity that ultimately exacerbates kidney damage [1]. The role of individual immune cell types in AKI has been mostly investigated in previous years. However, despite the successful results in experimental studies, treatments targeting a broad immune response have yielded minor improvements in patient outcomes, in part due to the imprecise understanding of immune cell heterogeneity. Recently, the focus of AKI research has shifted toward gaining insight into the heterogeneity and dynamic changes in immune cells with novel experimental approaches such as single-cell analysis, thereby redefining AKI pathophysiology.

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References

  1. Jang HR, Rabb H. Immune cells in experimental acute kidney injury. Nat Rev Nephrol. 2015;11:88–101.

    Article  CAS  PubMed  Google Scholar 

  2. Ryu S, Shin JW, Kwon S, Lee J, Kim YC, Bae YS, et al. Siglec-F-expressing neutrophils are essential for creating a profibrotic microenvironment in renal fibrosis. J Clin Invest. 2022;132:e156876.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Pan Y, Cao S, Terker AS, Tang J, Sasaki K, Wang Y, et al. Myeloid cyclooxygenase-2/prostaglandin E2/E-type prostanoid receptor 4 promotes transcription factor MafB-dependent inflammatory resolution in acute kidney injury. Kidney Int. 2022;101:79–91.

    Article  CAS  PubMed  Google Scholar 

  4. Leng J, Zhao W, Guo J, Yu G, Zhu G, Ge J, et al. E-prostanoid 3 receptor deficiency on myeloid cells protects against ischemic acute kidney injury via breaking the auto-amplification loop of necroinflammation. Kidney Int. 2023;103:100–14.

    Article  CAS  PubMed  Google Scholar 

  5. Yao W, Chen Y, Li Z, Ji J, You A, Jin S, et al. Single Cell RNA sequencing identifies a unique inflammatory macrophage subset as a druggable target for alleviating acute kidney injury. Adv Sci. 2022;9:e2103675.

    Article  Google Scholar 

  6. Deng B, Lin Y, Chen Y, Ma S, Cai Q, Wang W, et al. Plasmacytoid dendritic cells promote acute kidney injury by producing interferon-alpha. Cell Mol Immunol. 2021;18:219–29.

    Article  CAS  PubMed  Google Scholar 

  7. Salei N, Rambichler S, Salvermoser J, Papaioannou NE, Schuchert R, Pakalniskyte D, et al. The kidney contains ontogenetically distinct dendritic cell and macrophage subtypes throughout development that differ in their inflammatory properties. J Am Soc Nephrol. 2020;31:257–78.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Salei N, Ji X, Pakalniskyte D, Kuentzel V, Rambichler S, Li N, et al. Selective depletion of a CD64-expressing phagocyte subset mediates protection against toxic kidney injury and failure. Proc Natl Acad Sci USA. 2021;118:e2022311118.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Inaba A, Tuong ZK, Riding AM, Mathews RJ, Martin JL, Saeb-Parsy K, et al. CCL7 augments neutrophil and monocyte recruitment, exacerbating acute kidney injury. J Immunol. 2020;205:1376–84.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Sadasivam M, Noel S, Lee SA, Gong J, Allaf ME, Pierorazio P, et al. Activation and proliferation of PD-1(+) kidney double-negative T cells is dependent on nonclassical MHC Proteins and IL-2. J Am Soc Nephrol. 2019;30:277–92.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Gong J, Noel S, Hsu J, Bush EL, Arend LJ, Sadasivam M, et al. TCR(+)CD4(-)CD8(-) (double negative) T cells protect from cisplatin-induced renal epithelial cell apoptosis and acute kidney injury. Am J Physiol Ren Physiol. 2020;318:F1500–F1512.

    Article  CAS  Google Scholar 

  12. Cao Q, Wang R, Wang Y, Niu Z, Chen T, Wang C, et al. Regulatory innate lymphoid cells suppress innate immunity and reduce renal ischemia/reperfusion injury. Kidney Int. 2020;97:130–42.

    Article  CAS  PubMed  Google Scholar 

  13. do Valle Duraes F, Lafont A, Beibel M, Martin K, Darribat K, Cuttat R, et al. Immune cell landscaping reveals a protective role for regulatory T cells during kidney injury and fibrosis. JCI Insight. 2020;5:e130651.

    Article  PubMed  PubMed Central  Google Scholar 

  14. Dixon EE, Wu H, Muto Y, Wilson PC, Humphreys BD. Spatially resolved transcriptomic analysis of acute kidney injury in a female murine model. J Am Soc Nephrol. 2022;33:279–89.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Zhang M, Wu L, Deng Y, Peng F, Wang T, Zhao Y, et al. Single cell dissection of epithelial-immune cellular interplay in acute kidney injury microenvironment. Front Immunol. 2022;13:857025.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

This study was supported by grants from the Shanghai Sailing Program (No: 20YF1423400 to B.D.), the National Natural Science Foundation of China (No: 81870462, 82070789 to F.D.; No: 82200747 to B.D.; No: 32002153 to S.W.), the Shanghai Huangpu Industry Support Grant (XK2020002 to F.D.), the Collaborative Innovation Center for Clinical and Translational Science by Chinese Ministry of Education & Shanghai (CCTS-2022206 to F.D.), the Biomaterials & Regenerative Medicine Institute Cooperative Research Project (2022LHB01 to F.D.), the Clinical Research Program of 9th People’s Hospital (JYLJ202218 to F.D.), and the Postdoctoral Scientific Research Foundation of Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine (DengBo-2021-Scientific Research Start-up Funds to B.D.)

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Author notes

  1. These authors contributed equally: Bo Deng, Sutian Wang.

Authors and Affiliations

  1. Division of Nephrology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

    Bo Deng, Peihui Zhou & Feng Ding

  2. State Key Laboratory of Livestock and Poultry Breeding, Guangdong Key Laboratory of Animal Breeding and Nutrition, Institute of Animal Science, Guangdong Academy of Agricultural Sciences, Guangzhou, China

    Sutian Wang

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  1. Bo Deng
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  2. Sutian Wang
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  3. Peihui Zhou
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BD and SW wrote the manuscript. PZ drew the picture. FD designed and performed the final proofreading of the manuscript.

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Correspondence to Feng Ding.

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The authors declare no competing interests.

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Deng, B., Wang, S., Zhou, P. et al. New insights into immune cell diversity in acute kidney injury. Cell Mol Immunol 20, 680–682 (2023). https://doi.org/10.1038/s41423-023-01003-2

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