Journal
JOURNAL OF IMMUNOLOGY
Volume 193, Issue 12, Pages 5791-5800Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401768
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Funding
- Ministry of Education, Culture, Sports, Science and Technology
- Strategic Research Foundation at Private Universities [S1001055]
- Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (KAKENHI) [24790484, 26860340]
- Hyogo Science and Technology Association
- Grants-in-Aid for Scientific Research [26860340, 24790484, 26670480, 24390253] Funding Source: KAKEN
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Allergen-specific IgE is linked to asthma pathogenesis, but the underlying mechanisms of IgE production in response to allergen exposure are poorly understood. In this article, we show that B cell-intrinsic MyD88 is essential for IgE/IgG1 production evoked by ragweed pollen instilled into lungs. MyD88-deficient mice showed defective IgE/IgG1 production and germinal center responses to lung instillation of ragweed pollen. However, MyD88 was dispensable for dendritic cell activation and Th2 cell development. B cell-specific deletion of MyD88 replicated the defective Ab production observed in MyD88-deficient mice. Although ragweed pollen contains TLR ligands, TLR2/4/9-deficient mice developed normal allergic responses to ragweed pollen. However, anti-IL-1R1 Ab-treated mice and IL-18-deficient mice showed decreased IgE/IgG1 production with normal Th2 development. Furthermore, B cell-specific MyD88-deficient mice showed reduced IgE/IgG1 production in response to lung instillation of OVA together with IL-1 alpha, IL-1 beta, or IL-18. Thus, pollen instillation into lungs induces IL-1 alpha/beta and IL-18 production, which activates B cell-intrinsic MyD88 signaling to promote germinal center responses and IgE/IgG1 production.
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