期刊
IMMUNITY
卷 34, 期 4, 页码 514-526出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.019
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资金
- UOEH
- Ministry of Education, Science, Sports and Culture of Japan [21890297, 22791094]
- Grants-in-Aid for Scientific Research [21890297, 22791094, 21689015] Funding Source: KAKEN
Particulates such as silica crystal (silica) and aluminum salts (alum) activate the inflammasome and induce the secretion of proinflammatory cytokines in macrophages. These particulates also induce the production of immunoglobulin E via a T helper 2 (Th2) cell-associated mechanism. However, the mechanism involved in the induction of type 2 immunity has not been elucidated. Here, we showed that silica and alum induced lipopolysaccharide-primed macrophages to produce the lipid mediator prostaglandin E-2 (PGE(2)) and interleukin-1 beta (IL-1 beta). Macrophages deficient in the inflammasome components caspase 1, NALP3, and ASC revealed that PGE(2) production was independent of the NALP3 inflammasome. PGE(2) expression was markedly reduced in PGE synthase-deficient (Piges(-/-)) macrophages, and Ptges(-/-)mice displayed reduced antigen-specific serum IgE concentrations after immunization with alum or silica. Our results indicate that silica and alum regulate the production of PGE(2) and that the induction of PGE(2) by particulates controls the immune response in vivo.
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