| First Author | Ohno T | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 12 | Pages | 7890-7 |
| PubMed ID | 19933859 | Mgi Jnum | J:157483 |
| Mgi Id | MGI:4430961 | Doi | 10.4049/jimmunol.0802449 |
| Citation | Ohno T, et al. (2009) Caspase-1, caspase-8, and calpain are dispensable for IL-33 release by macrophages. J Immunol 183(12):7890-7 |
| abstractText | In addition to IL-1 and IL-18, IL-33 was recently identified as a member of the IL-1 cytokine family. rIL-33 can promote production of Th2-type cytokines by Th2 cells and mast cells in vitro. Administration of rIL-33 to mice results in increases in IgE secretion and eosinophilic inflammation. However, the precise immune cell source of IL-33 remains unclear. Moreover, although recombinant pro-IL-33 is cleaved by recombinant caspase-1 in vitro, as are pro-IL-1beta and pro-IL-18, the involvement of caspase-1 in pro-IL-33 cleavage remains controversial. In this study, we show that mouse peritoneal macrophages, but not splenic dendritic cells, produced IL-33 upon stimulation with LPS. Likewise, mouse bone marrow cell-derived cultured mast cells also produced a small, but significant amount of IL-33 via FcepsilonRI cross-linking, but not in response to stimulation with LPS. To our surprise, IL-33 release was found even in caspase-1-deficient, caspase-8 inhibitor-treated, and calpain inhibitor-treated macrophages. These observations suggest that caspase-1-, caspase-8-, and calpain-independent IL-33 production by macrophages and/or mast cells may contribute to the pathogenesis of Th2-type allergic inflammation. |
