Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 106, Issue 17, Pages 7119-7124Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0902745106
Keywords
cytokines; inflammasome; Th1; Th17; Th2
Categories
Funding
- National Institutes of Health, National Institute of Allergy and Infectious Diseases
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IL-1 causes a marked increase in the degree of expansion of naive and memory CD4 T cells in response to challenge with their cognate antigen. The response occurs when only specific CD4 T cells can respond to IL-1 beta, is not induced by a series of other cytokines and does not depend on IL-6 or CD-28. When WT cells are primed in IL-1R1(-/-) recipients, IL-1 increases the proportion of cytokine-producing transgenic CD4 T cells, especially IL-17- and IL-4-producing cells, strikingly increases serum IgE levels and serum IgG1 levels. IL-1 beta enhances antigen-mediated expansion of in vitro primed Th1, Th2, and Th17 cells transferred to IL-1R1(-/-) recipients. The IL-1 receptor antagonist diminished responses to antigen plus lipopolysaccharide (LPS) by approximate to 55%. These results indicate that IL-1 beta signaling in T cells markedly induces robust and durable primary and secondary CD4 responses.
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