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

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2009年 / 106卷 / 17期

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

页码：7119 / 7124

页数：6

共 36 条

[1] Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells [J].