Journal
SCIENCE
Volume 335, Issue 6068, Pages 597-601Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1215173
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Funding
- NIH [1R01HL095612, U01 HL080731, P50 CA86355, R24 CA69246, P01-A154904]
- Boehringer Ingelheim Fonds
- American Heart Association
- MGH Executive Committee on Research (ECOR)
- German Research Foundation
- Max Kade Foundation
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Recognition and clearance of a bacterial infection are fundamental properties of innate immunity. Here, we describe an effector B cell population that protects against microbial sepsis. Innate response activator (IRA) B cells are phenotypically and functionally distinct, develop and diverge from B1a B cells, depend on pattern-recognition receptors, and produce granulocyte-macrophage colony-stimulating factor. Specific deletion of IRA B cell activity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock. These observations enrich our understanding of innate immunity, position IRA B cells as gatekeepers of bacterial infection, and identify new treatment avenues for infectious diseases.
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