A new study shows how the cytokine interleukin-9 (IL-9) indirectly promotes tissue repair after worm-induced inflammatory damage in the lung by inducing the survival and activation of type 2 innate lymphoid cells (ILC2s) (J. Exp. Med. 210, 2951–2965, 2013).
Previous studies showed that ILC2s produce IL-9 during lung inflammation and contribute to host immunity in helminth infection in the gut. Jan-Eric Turner and his colleagues found that ILC2s in lungs are also the main producers of IL-9 in response to tissue damage caused during the lung stage of a worm infection. Using mice lacking the IL-9 receptor, the authors also showed that accumulation of ILC2s—but not T helper type 2 cells—during worm-induced lung injury requires IL-9, which induces the antiapoptotic protein BCL3. In ILC2s, this IL-9–mediated autocrine survival signal resulted in increased secretion of type 2 cytokines and amphiregulin and recruitment and activation of myeloid cells, which in concert promote lung damage repair at chronic stages.
Future studies should clarify how this IL-9 feedback loop may be halted after repair to clear ILC2s from the lungs to prevent potential harmful effects of these cells in the lung.
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Pola, C. Post-worm lung repair. Nat Med 20, 128 (2014). https://doi.org/10.1038/nm.3476
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DOI: https://doi.org/10.1038/nm.3476