Allergen-induced airway hyperreactivity is diminished in CD81-deficient mice

被引:39
作者
Deng, J
Yeung, VP
Tsitoura, D
DeKruyff, RH
Umetsu, DT
Levy, S
机构
[1] Stanford Univ, Med Ctr, Dept Med, Div Oncol, Stanford, CA 94305 USA
[2] Stanford Univ, Med Ctr, Dept Pediat, Div Immunol & Transplantat Biol, Stanford, CA 94305 USA
关键词
D O I
10.4049/jimmunol.165.9.5054
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We demonstrated previously that CD81(-/-) mice have an impaired Th2 response. To determine whether this impairment affected allergen-induced airway hyperreactivity (AHR), CD81(-/-) BALB/c mice and CD81(+/+) littermates were sensitized i.p. and challenged intranasally with OVA, Although wild type developed severe AHR, CD81(-/-) mice showed normal airway reactivity and reduced airway inflammation. Nevertheless, OVA-specific T cell proliferation was similar in both groups of mice, Analysis of cytokines secreted by the responding CD81(-/-) T cells, particularly those derived from peribronchial draining lymph nodes, revealed a dramatic reduction in IL-4, IL-5, and IL-13 synthesis. The decrease in cytokine production was not due to an intrinsic T cell deficiency because naive CD81(-/-) T cells responded to polyclonal Th1 and Th2 stimulation with normal proliferation and cytokine production. Moreover, there was an increase in T cells and a decrease in B cells in peribronchial lymph nodes and in spleens of immunized CD81(-/-) mice compared with wild-type animals. Interestingly OVA-specific Ig levels, including IgE, were similar in CD81(-/-) and CD81(+/+) mice. Thus, CD81 plays a role in the development of AHR not by influencing Ag-specific IgE production but by regulating local cytokine production.
引用
收藏
页码:5054 / 5061
页数:8
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