Cutting edge: B and T lymphocyte attenuator and programmed death receptor-1 inhibitory receptors are required for termination of acute allergic airway inflammation

被引:79
作者
Deppong, Christine
Juehne, Twyla I.
Hurchla, Michelle
Friend, Lindzy D.
Shah, Dulari D.
Rose, Christine M.
Bricker, Traci L.
Shornick, Laurie P.
Crouch, Erika C.
Murphy, Theresa L.
Holtzman, Michae J.
Murphy, Kenneth M.
Green, Jonathan M.
机构
[1] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Program Immunol, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA
[4] Washington Univ, Sch Med, Dept Cell Biol, St Louis, MO 63110 USA
[5] Washington Univ, Sch Med, Howard Hughes Med Inst, St Louis, MO 63110 USA
关键词
D O I
10.4049/jimmunol.176.7.3909
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
T cell activation is regulated by coordinate interaction of the T cell Ag receptor and costimulatory signals. Although there is considerable insight into processes that regulate the initiation of inflammation, less is known about the signals that terminate immune responses. We have examined the role of the inhibitory receptors programmed death receptor-1 and B and T lymphocyte attenuator in the regulation of allergic airway inflammation. Our results demonstrate that there is a temporally regulated expression of both the receptors and their ligands during the course of allergic airway inflammation. Following a single inhaled challenge, sensitized wild-type mice exbibit peak inflammation on day 3, which resolves by day 10. In contrast, mice deficient in the expression of programmed death receptor-1 or B and T lymphocyte attenuator have persistent inflammation out to 15 days following challenge. Thus, these receptors are critical determinants of the duration of allergic airway inflammation.
引用
收藏
页码:3909 / 3913
页数:5
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