Cutting edge: LFA-1 interaction with ICAM-1 and ICAM-2 regulates Th2 cytokine production

被引：0
|
作者：
Salomon, B
Bluestone, JA
机构：
[1] Univ Chicago, Ben May Inst Canc Res, Dept Pathol, Chicago, IL 60637 USA
[2] Univ Chicago, Comm Immunol, Chicago, IL 60637 USA
来源：
JOURNAL OF IMMUNOLOGY | 1998年 / 161卷 / 10期
关键词：
D O I：
暂无
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The role of CD28/B7 and LFA-1/ICAM costimulation in proliferation and Th1/Th2 differentiation of naive CD4(+) T cells was addressed using T cells from DO11.10 TCR transgenic mice stimulated by dendritic cells. The blockade of either CD28/B7 or LFA-1/ICAM interactions partially inhibited T cell proliferation. By comparison, blocking CD28/B7 costimulation inhibited IL-4 and IL-5 (Th2 cytokine) production, whereas blocking LFA-1/ICAM-1 or LFA-1/ICAM-2 led to a significant increase (15- to 40-fold) of Th2 cytokines. The combination of anti-ICAM-1 and anti-ICAM-2 mAbs had a synergistic effect with a 100- to 1000-fold increase of Th2 cytokine production. Thus, these two costimulatory pathways have opposing roles in the regulation of Th2 development.
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页码：5138 / 5142
页数：5
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