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Contribution of IL-33–activated type II innate lymphoid cells to pulmonary eosinophilia in intestinal nematode-infected mice

Yasuda, Koubun, Muto, Taichiro, Kawagoe, Tatsukata, Matsumoto, Makoto, Sasaki, Yuki, Matsushita, Kazufumi, Taki, Yuko, Futatsugi-Yumikura, Shizue, Tsutsui, Hiroko, Ishii, Ken J., Yoshimoto, Tomohiro, Akira, Shizuo, Nakanishi, Kenji
Proceedings of the National Academy of Sciences of the United States of America 2012 v.109 no.9 pp. 3451-3456
Strongyloides, eosinophilia, hosts, immune response, inflammation, interleukin-5, intranasal administration, lungs, mice, parasites
When animals are infected with helminthic parasites, resistant hosts show type II helper T immune responses to expel worms. Recently, natural helper (NH) cells or nuocytes, newly identified type II innate lymphoid cells, are shown to express ST2 (IL-33 receptor) and produce IL-5 and IL-13 when stimulated with IL-33. Here we show the relevant roles of endogenous IL-33 for Strongyloides venezuelensis infection-induced lung eosinophilic inflammation by using Il33–/– mice. Alveolar epithelial type II cells (ATII) express IL-33 in their nucleus. Infection with S. venezuelensis or intranasal administration of chitin increases in the number of ATII cells and the level of IL-33. S. venezuelensis infection induces pulmonary accumulation of NH cells, which, after being stimulated with IL-33, proliferate and produce IL-5 and IL-13. Furthermore, S. venezuelensis infected Rag2–/– mice increase the number of ATII cells, NH cells, and eosinophils and the expression of IL-33 in their lungs. Finally, IL-33–stimulated NH cells induce lung eosinophilic inflammation and might aid to expel infected worms in the lungs.