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* Department of Chemical Pathology, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong; and
Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology Foundation, Macau, China
IL-17A and IL-17F are members of the IL-17 family that play crucial roles in allergic inflammation. Recent studies reported that IL-17A and IL-17F production from a distinct Th lymphocyte subset, Th17, was specifically induced by IL-23, which was produced by dendritic cells and macrophages in response to microbial stimuli. The IL-23-IL-17 axis might therefore provide a link between infections and allergic diseases. In the present study, we investigated the effects of IL-17A, IL-17F, and IL-23, alone or in combination, on cytokine and chemokine release from eosinophils and the underlying intracellular mechanisms. Human eosinophils were found to constitutively express receptors for IL-17A, IL-17F, and IL-23 at the protein level. IL-17A, IL-17F, and IL-23 could induce the release of chemokines GRO-
/CXCL1, IL-8/CXCL8, and MIP-1β/CCL4 from eosinophils, while IL-17F and IL-23 could also increase the production of proinflammatory cytokines IL-1β and IL-6. Synergistic effects were observed in the combined treatment of IL-17F and IL-23 on the release of proinflammatory cytokines, and the effects were dose-dependently enhanced by IL-23, but not IL-17F. Further investigations showed that IL-17A, IL-17F, and IL-23 differentially activated the ERK, p38 MAPK, and NF-
B pathways. Moreover, inhibition of these pathways using selective inhibitors could significantly abolish the chemokine release induced by IL-17A, IL-17F, and IL-23 and the synergistic increases on IL-1β and IL-6 production mediated by combined treatment of IL-17F and IL-23. Taken together, our findings provide insight for the Th17 lymphocyte-mediated activation of eosinophils via differential intracellular signaling cascades in allergic inflammation.
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1 P.F.Y.C. and C.K.W. share first authorship.
2 Address correspondence and reprint requests to Dr. Christopher W. K. Lam, Department of Chemical Pathology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong, China. E-mail address: waikeilam{at}cuhk.edu.hk
3 Abbreviations used in this paper: MFI, mean fluorescence intensity; PI, propidium iodide.
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