Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 12, Pages 7890-7897Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802449
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Funding
- National Institute of Biomedical Innovation [ID 05-24]
- Ministry of Health, Labour, and Welfare, Research on Allergic Disease and Immunology [21200201]
- Ministry of Education, Culture, Sports, Science, and Technology [21390303, 18790694, 18890236]
- Grants-in-Aid for Scientific Research [18790694, 21390303, 18890236] Funding Source: KAKEN
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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 or IL-33 remains unclear. Moreover, although recombinant pro-IL-33 is cleaved by recombinant caspase-1 in vitro, as are pro-IL-1 beta 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 Fc epsilon RI 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. The Journal of Immunology, 2009, 183: 7890-7897.
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