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Stop Press: Eosinophils Drafted to Join the Th17 Team.
1Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute and University of Newcastle, Newcastle, New South Wales, 2308, Australia.
Immunity
|July 23, 2015
Summary
Eosinophils play a novel role in colitis, independent of Th2 immunity. Researchers discovered a new granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent function for eosinophils in interleukin-23 (IL-23)-induced Th17 cell colitis.
Area of Science:
- Immunology
- Inflammation research
- Gastroenterology
Background:
- Eosinophils are traditionally linked to T-helper 2 (Th2) cell-mediated inflammatory conditions.
- The specific roles of eosinophils in other immune responses, such as T-helper 17 (Th17) cell-driven inflammation, remain less understood.
Purpose of the Study:
- To investigate the role of eosinophils in the pathogenesis of interleukin-23 (IL-23)-induced colitis, a model of Th17 cell-driven inflammation.
- To identify potential mechanisms by which eosinophils contribute to this specific inflammatory disease.
Main Methods:
- The study utilized a mouse model of IL-23-induced colitis.
- Investigated the involvement of eosinophils and granulocyte-macrophage colony-stimulating factor (GM-CSF) in disease development.
- Employed techniques to assess inflammatory markers and cellular infiltration in the colon.
Main Results:
- Eosinophils were found to be crucial in the pathogenesis of IL-23-induced Th17 cell colitis.
- A novel, GM-CSF-dependent function for eosinophils was identified in this context.
- These findings indicate a role for eosinophils beyond Th2-driven inflammation.
Conclusions:
- Eosinophils contribute to the development of IL-23-induced Th17 cell colitis through a GM-CSF-dependent mechanism.
- This study expands the known functions of eosinophils, highlighting their involvement in Th17-mediated inflammatory diseases.
