Journal article
Cameron GJM, Cautivo KM, Loering S, Jiang SH, Deshpande AV, Foster PS, McKenzie ANJ, Molofsky AB, Hansbro PM, Starkey MR.
Front Immunol, vol. 10(1), 2019, p. 826
Front Immunol, vol. 10(1), 2019, p. 826
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GJM, C., KM, C., S, L., SH, J., AV, D., PS, F., … MR., S. (2019). Group 2 innate lymphoid cells are redundant in experimental renal ischemia-reperfusion injury. Front Immunol, 10(1), 826. https://doi.org/10.3389/fimmu.2019.00826
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GJM, Cameron, Cautivo KM, Loering S, Jiang SH, Deshpande AV, Foster PS, McKenzie ANJ, Molofsky AB, Hansbro PM, and Starkey MR. “Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury.” Front Immunol 10, no. 1 (2019): 826.
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GJM, Cameron, et al. “Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury.” Front Immunol, vol. 10, no. 1, 2019, p. 826, doi:10.3389/fimmu.2019.00826.
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@article{cameron2019a,
title = {Group 2 innate lymphoid cells are redundant in experimental renal ischemia-reperfusion injury},
year = {2019},
issue = {1},
journal = {Front Immunol},
pages = {826},
volume = {10},
doi = {10.3389/fimmu.2019.00826},
author = {GJM, Cameron and KM, Cautivo and S, Loering and SH, Jiang and AV, Deshpande and PS, Foster and ANJ, McKenzie and AB, Molofsky and PM, Hansbro and MR., Starkey}
}
Abstract
Acute kidney injury (AKI) can be fatal and is a well-defined risk factor for the development of chronic kidney disease. Group 2 innate lymphoid cells (ILC2s) are innate producers of type-2 cytokines and are critical regulators of homeostasis in peripheral organs. However, our knowledge of their function in the kidney is relatively limited. Recent evidence suggests that increasing ILC2 numbers by systemic administration of recombinant interleukin (IL)-25 or IL-33 protects against renal injury. Whilst ILC2s can be induced to protect against ischemic- or chemical-induced AKI, the impact of ILC2 deficiency or depletion on the severity of renal injury is unknown. Firstly, the phenotype and location of ILC2s in the kidney was assessed under homeostatic conditions. Kidney ILC2s constitutively expressed high levels of IL-5 and were located in close proximity to the renal vasculature. To test the functional role of ILC2s in the kidney, an experimental model of renal ischemia-reperfusion injury (IRI) was used and the severity of injury was assessed in wild-type, ILC2-reduced, ILC2-deficient, and ILC2-depleted mice. Surprisingly, there were no differences in histopathology, collagen deposition or mRNA expression of injury-associated (Lcn2), inflammatory (Cxcl1, Cxcl2, and Tnf) or extracellular matrix (Col1a1, Fn1) factors following IRI in the absence of ILC2s. These data suggest the absence of ILC2s does not alter the severity of renal injury, suggesting possible redundancy. Therefore, other mechanisms of type 2-mediated immune cell activation likely compensate in the absence of ILC2s. Hence, a loss of ILC2s is unlikely to increase susceptibility to, or severity of AKI.
Keywords: IL-13; IL-5; ILC2; IRI; group 2 innate lymphoid cell; ischemia-reperfusion injury; kidney; renal.
Copyright © 2019 Frontiers Media S.A.
Keywords: IL-13; IL-5; ILC2; IRI; group 2 innate lymphoid cell; ischemia-reperfusion injury; kidney; renal.
Copyright © 2019 Frontiers Media S.A.
