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Comment
. 2020 Nov;13(6):849-851.
doi: 10.1038/s41385-020-0329-z. Epub 2020 Jul 29.

IL-17A moonlighting in lung type 2 immunity

Roland Ruscher  1 , Paul R Giacomin  2
Affiliations
Comment

IL-17A moonlighting in lung type 2 immunity

Roland Ruscher et al. Mucosal Immunol. 2020 Nov.
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Pulmonary responses to helminth infections.
Under homeostatic conditions, T cell and natural killer (NK) cell derived IFNγ keeps Type 2 immunity in check by suppressing Th2 cell and ILC2 responses. However, in the early stages (day 2) following infection with N. brasiliensis, IL-17A secreted by γδ T cells inhibits IFNγ production, thereby facilitating initiation of a Type 2 response. During later infection (day 6), IL-17A acts instead to suppress this Type 2 response, preventing excessive inflammation and tissue damage. The source of IL-17A and the mechanism of suppression of Type 2 immunity remain unclear. This IL-17A-dependent molecular switch adds to previously characterized mechanisms of how Type 2 immunity in the lung is regulated during helminth infections, including the similarly multitasking factor RELMα, produced by alternatively activated macrophages (AAMac), which can both promote early Type 2 responses to helminths, and act to suppress these responses at later times., Similarly, induction of regulatory T-cell (Treg) responses by helminths is associated with suppression of pulmonary Type 2 responses, which can be effective at limiting house dust mite-induced asthma, and limit Th2 cell-dependent protective immunity.
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References

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