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

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.

Automated summary

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestine with a complex etiology involving genetics, gut microbiome, environment, and immune system. Recent research has suggested that innate lymphoid cells (ILCs) may play a significant role in the dysregulation of intestinal immunity observed in IBD. Despite being rare in the intestine, helper-like ILCs may contribute to the exacerbation of IBD pathology.