Summary
This narrative review synthesises current understanding of type 17 immunity—orchestrated by IL-23 signalling in innate and adaptive immune cells—and its dual role in maintaining intestinal homeostasis and driving chronic inflammatory disease. The authors examine how these proinflammatory cytokines (IL-17, IL-22, GM-CSF) support mucosal defence but, when dysregulated, contribute to inflammatory bowel disease, autoimmune arthritis, and neuroinflammation through gut-primed T cell responses. The review emphasises the complexity of type 17 immunity across diverse infection and inflammation models, highlighting its cross-organ pathogenic effects in autoimmunity.
Regional applicability
This is a mechanistic immunology review with no specific geographical focus; findings on gut immunity and autoimmune pathogenesis are relevant to United Kingdom clinical and research contexts. The pathways and disease models discussed (IBD, autoimmune arthritis) are globally prevalent and not geographically limited.
Key measures
IL-23 signaling pathway activity; secretion of IL-17, IL-22, and GM-CSF; intestinal barrier integrity; mucosal immune responses; inflammatory markers in colitis and infection models; autoimmune disease pathogenesis
Outcomes reported
The review examines the roles of IL-23 signaling and type 17 cytokines (IL-17, IL-22, GM-CSF) in maintaining intestinal immune equilibrium and mucosal defence, and their involvement in chronic inflammatory disorders including inflammatory bowel diseases and autoimmunity. It focuses on how gut-primed T cells drive autoimmune arthritis and neuroinflammation across multiple organs.
Topic tags
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