| First Author | Shimura E | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 453 |
| Issue | 1 | Pages | 1-6 |
| PubMed ID | 25204502 | Mgi Jnum | J:220092 |
| Mgi Id | MGI:5632229 | Doi | 10.1016/j.bbrc.2014.09.004 |
| Citation | Shimura E, et al. (2014) Potential role of myeloid cell/eosinophil-derived IL-17 in LPS-induced endotoxin shock. Biochem Biophys Res Commun 453(1):1-6 |
| abstractText | IL-17RA is a shared receptor subunit for several cytokines of the IL-17 family, including IL-17A, IL-17C, IL-17E (also called IL-25) and IL-17F. It has been shown that mice deficient in IL-17RA are more susceptible to sepsis than wild-type mice, suggesting that IL-17RA is important for host defense against sepsis. However, it is unclear which ligands for IL-17RA, such as IL-17A, IL-17C, IL-17E/IL-25 and/or IL-17F, are involved in the pathogenesis of sepsis. Therefore, we examined IL-17A, IL-17E/IL-25 and IL-17F for possible involvement in LPS-induced endotoxin shock. IL-17A-deficient mice, but not IL-25- or IL-17F-deficient mice, were resistant to LPS-induced endotoxin shock, as compared with wild-type mice. Nevertheless, studies using IL-6-deficient, IL-21Ralpha-deficient and Rag-2-deficient mice, revealed that neither IL-6 and IL-21, both of which are important for Th17 cell differentiation, nor Th17 cells were essential for the development of LPS-induced endotoxin shock, suggesting that IL-17A-producing cells other than Th17 cells were important in the setting. In this connection, IL-17A was produced by macrophages, DCs and eosinophils after LPS injection. Taken together, these findings indicate that IL-17A, but not IL-17F or IL-25, is crucial for LPS-induced endotoxin shock. In addition, macrophages, DCs and eosinophils, but not Th17 cells or gammadelta T cells, may be sources of IL-17A during LPS-induced endotoxin shock. |
