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Helper-Like Type-1 Innate Lymphoid Cells in Inflammatory Bowel Disease

Research output: Contribution to journalReview articlepeer-review

Original languageEnglish
Article number903688
JournalFrontiers in immunology
Accepted/In press17 May 2022
Published23 Jun 2022

Bibliographical note

Funding Information: DC acknowledges a Ph.D. studentship from the National Institute of Health and Care Research (NIHR) Biomedical Research Centre (BRC) based at Guy’s and St Thomas’ (GSTT) NHS Foundation Trust and King’s College London (KCL), and LR is also supported by NIHR BRC based at GSTT and KCL. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care. We apologize to authors whose papers we could not include due to space and scope limitations. Publisher Copyright: Copyright © 2022 Coman, Coales, Roberts and Neves.

King's Authors


Inflammatory bowel disease (IBD) is an idiopathic condition characterized by chronic relapsing inflammation in the intestine. While the precise etiology of IBD remains unknown, genetics, the gut microbiome, environmental factors, and the immune system have all been shown to contribute to the disease pathophysiology. In recent years, attention has shifted towards the role that innate lymphoid cells (ILCs) may play in the dysregulation of intestinal immunity observed in IBD. ILCs are a group of heterogenous immune cells which can be found at mucosal barriers. They act as critical mediators of the regulation of intestinal homeostasis and the orchestration of its inflammatory response. Despite helper-like type 1 ILCs (ILC1s) constituting a particularly rare ILC population in the intestine, recent work has suggested that an accumulation of intestinal ILC1s in individuals with IBD may act to exacerbate its pathology. In this review, we summarize existing knowledge on helper-like ILC1 plasticity and their classification in murine and human settings. Moreover, we discuss what is currently understood about the roles that ILC1s may play in the progression of IBD pathogenesis.

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