AI Article Synopsis
- T helper 9 (Th9) cells produce interleukin-9 (IL-9), contributing to lung inflammation and allergies, but the exact mechanisms of IL-9's role were previously unclear.
- Research reveals an IL-9-driven feedback loop that enhances allergic inflammation, where IL-9 stimulates mast cells to produce IL-2, which further promotes the activation of Th9 cells.
- Overproduction of IL-9 is linked to cystic fibrosis patients, with a specific variant of IL-9 predicting allergic reactions in women, suggesting that targeting IL-9 could be a potential treatment to reduce lung inflammation.
Article Abstract
T helper 9 (Th9) cells contribute to lung inflammation and allergy as sources of interleukin-9 (IL-9). However, the mechanisms by which IL-9/Th9 mediate immunopathology in the lung are unknown. Here we report an IL-9-driven positive feedback loop that reinforces allergic inflammation. We show that IL-9 increases IL-2 production by mast cells, which leads to expansion of CD25 type 2 innate lymphoid cells (ILC2) and subsequent activation of Th9 cells. Blocking IL-9 or inhibiting CD117 (c-Kit) signalling counteracts the pathogenic effect of the described IL-9-mast cell-IL-2 signalling axis. Overproduction of IL-9 is observed in expectorates from cystic fibrosis (CF) patients, and a sex-specific variant of IL-9 is predictive of allergic reactions in female patients. Our results suggest that blocking IL-9 may be a therapeutic strategy to ameliorate inflammation associated with microbial colonization in the lung, and offers a plausible explanation for gender differences in clinical outcomes of patients with CF.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5241810 | PMC |
| http://dx.doi.org/10.1038/ncomms14017 | DOI Listing |
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