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Th17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics
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DOI：10.1186/s12974-026-03993-y.png)
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Abstract
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Substantial evidence from human studies and experimental mouse models highlights a key role for dysregulated Th17 cell responses in the pathogenesis of chronic inflammatory disorders, including neuroinflammatory conditions such as multiple sclerosis (MS). Th17 cell biology is closely linked to neutrophils, with Th17 cells promoting optimal neutrophil effector functions and conversely, neutrophils propagating Th17 responses, indicating bi-directional Th17 neutrophil crosstalk is necessary for optimal type 17 immunity. Importantly, recent studies demonstrate communication networks between neutrophils and Th17 cell responses in numerous chronic inflammatory disorders suggesting that dysregulation of this interplay contributes to disease pathogenesis. This review discusses the current understanding of Th17-neutrophil bi-directional crosstalk and focusses specifically on how dysregulation of this interplay may drive chronic inflammation during central nervous system (CNS) autoimmunity. Furthermore, we consider how evolving therapeutics could exploit these interactions for the development of new treatment strategies.
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