IL-1 acts directly on CD4 T cells to enhance their antigen-driven expansion and differentiation

被引:455
作者
Ben-Sasson, Shlomo Z. [1 ,2 ]
Hu-Li, Jane [1 ]
Quiel, Juan [1 ]
Cauchetaux, Stephane [1 ]
Ratner, Maya [2 ]
Shapira, Ilana [2 ]
Dinarello, Charles A. [3 ]
Paul, William E. [1 ]
机构
[1] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA
[2] Hebrew Univ Jerusalem, Hadassah Med Ctr, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel
[3] Univ Colorado, Hlth Sci Ctr, Dept Infect Dis, Denver, CO 80045 USA
基金
美国国家卫生研究院;
关键词
cytokines; inflammasome; Th1; Th17; Th2; INTERLEUKIN-1 RECEPTOR ANTAGONIST; HOST-DEFENSE; DENDRITIC CELLS; EXPRESSION; RESPONSES; MICE; ACTIVATION; INFECTION; MECHANISM; IMMUNITY;
D O I
10.1073/pnas.0902745106
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:7119 / 7124
页数:6
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