Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury

Guy J.M. Cameron, Simon H. Jiang, Svenja Loering, Aniruddh V. Deshpande, Philip M. Hansbro, Malcolm R. Starkey

Research output: Contribution to journalReview ArticleResearchpeer-review

15 Citations (Scopus)


Acute kidney injury (AKI) remains a global challenge and, despite the availability of dialysis and transplantation, can be fatal. Those that survive an AKI are at increased risk of developing chronic kidney disease and end stage renal failure. Understanding the fundamental mechanisms underpinning the pathophysiology of AKI is critical for developing novel strategies for diagnosis and treatment. A growing body of evidence indicates that amplifying type 2 immunity may have therapeutic potential in kidney injury and disease. Of particular interest are the recently described subset of innate immune cells, termed group 2 innate lymphoid cells (ILCs). Group 2 ILCs are crucial tissue-resident immune cells that maintain homeostasis and regulate tissue repair at multiple organ sites, including the kidney. They are critical mediators of type 2 immune responses following infection and injury. The existing literature suggests that activation of group 2 ILCs and production of a local type 2 immune milieu is protective against renal injury and associated pathology. In this review, we describe the emerging role for group 2 ILCs in renal homeostasis and repair. We provide an in-depth discussion of the most recent literature that use preclinical models of AKI and assess the therapeutic effect of modulating group 2 ILC function. We debate the potential for targeting these cells as novel cellular therapies in AKI and discuss the implications for future studies and translation.

Original languageEnglish
Pages (from-to)9-15
Number of pages7
JournalJournal of Pathology
Issue number1
Publication statusPublished - May 2019
Externally publishedYes


  • acute kidney injury
  • alternatively activated macrophages
  • group 2 innate lymphoid cell
  • ILC2
  • innate immunity
  • ischemia–reperfusion injury
  • type 2 immunity

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