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Proc Natl Acad Sci U S A ; 106(17): 7119-24, 2009 Apr 28.
Article in English | MEDLINE | ID: mdl-19359475

ABSTRACT

IL-1 causes a marked increase in the degree of expansion of naïve 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-1beta, 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-1beta 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 approximately 55%. These results indicate that IL-1beta signaling in T cells markedly induces robust and durable primary and secondary CD4 responses.


Subject(s)
Antigens/immunology , CD4-Positive T-Lymphocytes/cytology , CD4-Positive T-Lymphocytes/immunology , Cell Differentiation/immunology , Interleukin-1/immunology , Animals , CD28 Antigens/immunology , Cell Proliferation , Female , Immunoglobulins/immunology , Immunologic Memory/immunology , Interleukin-17/immunology , Interleukin-6/immunology , Mice , Mice, Knockout , Receptors, Interleukin-1 Type I/deficiency , Receptors, Interleukin-1 Type I/genetics , Receptors, Interleukin-1 Type I/immunology , Receptors, Interleukin-1 Type I/metabolism
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