Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury

Group 2 Innate Lymphoid Cells Are Redundant in Experimental Renal Ischemia-Reperfusion Injury.

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Item Type: Article
Status: Published
Official URL: https://doi.org/10.3389/fimmu.2019.00826
Journal or Publication Title: Frontiers in Immunology
Volume: 10
Date: 2019
Divisions: UTS Centre for Inflammation
Depositing User: General Admin
Identification Number: 10.3389/fimmu.2019.00826
ISSN: 1664-3224
Date Deposited: 21 Dec 2020 06:02
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.

Creators:
Creators
Email
Cameron, Guy J. M.
UNSPECIFIED
Cautivo, Kelly M.
UNSPECIFIED
Loering, Svenja
UNSPECIFIED
Jiang, Simon H.
UNSPECIFIED
Deshpande, Aniruddh V.
UNSPECIFIED
Foster, Paul S.
UNSPECIFIED
McKenzie, Andrew N. J.
UNSPECIFIED
Molofsky, Ari B.
UNSPECIFIED
Hansbro, Philip M.
UNSPECIFIED
Starkey, Malcolm R.
UNSPECIFIED
Last Modified: 21 Dec 2020 06:02
URI: https://eprints.centenary.org.au/id/eprint/236

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