AI Article Synopsis
- Th17 cells are versatile immune cells that can adapt their functions while maintaining their identity, sometimes resembling stem cells.
- This study uses a mouse model to show that lung dendritic cells produce IL-2 through NFAT signaling, which is crucial for a protective Th17 response against invasive pulmonary aspergillosis.
- Lack of IL-2 in these dendritic cells leads to excessive IL-23 production, resulting in severe inflammation and the development of a Th17 stem-cell-like phenotype, highlighting the importance of the IL-2 and IL-23 balance in managing inflammation during infections.
Article Abstract
Th17 cells express diverse functional programs while retaining their Th17 identity, in some cases exhibiting a stem-cell-like phenotype. Whereas the importance of Th17 cell regulation in autoimmune and infectious diseases is firmly established, the signaling pathways controlling their plasticity are undefined. Using a mouse model of invasive pulmonary aspergillosis, we found that lung CD103(+) dendritic cells (DCs) would produce IL-2, dependent on NFAT signaling, leading to an optimally protective Th17 response. The absence of IL-2 in DCs caused unrestrained production of IL-23 and fatal hyperinflammation, which was characterized by strong Th17 polarization and the emergence of a Th17 stem-cell-like population. Although several cell types may be affected by deficient IL-2 production in DCs, our findings identify the balance between IL-2 and IL-23 productions by lung DCs as an important regulator of the local inflammatory response to infection.
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| http://dx.doi.org/10.1016/j.celrep.2015.08.030 | DOI Listing |
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