Th17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics
- 1The John Curtin School of Medical Research, The Australian National University, Canberra, ACT Australia
- 2School of Biological Sciences, College of Science, Adelaide University, Adelaide, SA 5005 Australia
Abstract
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.
Related
- Targeting NOTCH-immune crosstalk in gliomas: from mechanisms to therapeutics.
- Functional characterization of neutrophils in patients with multiple myeloma
- Baclofen for Spasticity in Multiple Sclerosis: A Comprehensive Narrative Review
- A 35-Year-Old Woman With Multiple Sclerosis and a New Atypical Thalamic Lesion: A Case Report From the National Multiple Sclerosis Society Case Conference Proceedings.
- Chronic lesion expansion persists in secondary progressive multiple sclerosis and is associated with neurodegeneration
BibTeX
@article{martin2026th17,
title = {{Th17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics}},
author = {Jacob V Martin and Caleb Wong Han and Anne Brüstle and Iain Comerford},
journal = {Journal of Neuroinflammation},
year = {2026},
month = aug,
doi = {10.1186/s12974-026-03993-y},
url = {https://doi.org/10.1186/s12974-026-03993-y},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Th17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics
AU - Jacob V Martin
AU - Caleb Wong Han
AU - Anne Brüstle
AU - Iain Comerford
PY - 2026
DA - 2026/08/07
JO - Journal of Neuroinflammation
DO - 10.1186/s12974-026-03993-y
UR - https://doi.org/10.1186/s12974-026-03993-y
AB - 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.
SN - 1742-2094
ER -