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B7-H3 contributes to the development of pathogenic Th2 cells in a murine model of asthma
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作者:

Nagashima, Osamu
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
Juntendo Univ, Sch Med, Dept Resp Med, Tokyo 1138421, Japan
Juntendo Univ, Sch Med, Res Inst Dis Old Ages, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Harada, Norihiro
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
Juntendo Univ, Sch Med, Dept Resp Med, Tokyo 1138421, Japan
Juntendo Univ, Sch Med, Res Inst Dis Old Ages, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Usui, Yoshihiko
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
Tokyo Med Univ, Dept Ophthalmol, Tokyo, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Yamazaki, Tomohide
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Yagita, Hideo
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Okumura, Ko
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Takahashi, Kazuhisa
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Juntendo Univ, Sch Med, Dept Resp Med, Tokyo 1138421, Japan
Juntendo Univ, Sch Med, Res Inst Dis Old Ages, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan

Akiba, Hisaya
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Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
机构:
[1] Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
[2] Juntendo Univ, Sch Med, Dept Resp Med, Tokyo 1138421, Japan
[3] Juntendo Univ, Sch Med, Res Inst Dis Old Ages, Tokyo 1138421, Japan
[4] Tokyo Med Univ, Dept Ophthalmol, Tokyo, Japan
关键词:
D O I:
10.4049/jimmunol.181.6.4062
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
B7-H3 is a new member of the B7 family. The receptor for B7-H3 has not been identified, but it seems to be expressed on activated T cells. Initial studies have shown that B7-H3 provides a stimulatory signal to T cells. However, recent studies suggest a negative regulatory role for B7-H3 in T cell responses. Thus, the immunological function of B7-H3 is controversial and unclear. In this study, we investigated the effects of neutralizing anti-B7-H3 mAb in a mouse model of allergic asthma to determine whether B7-H3 contributes to the development of pathogenic Th2 cells and pulmonary inflammation. Administration of anti-B7-H3 mAb significantly reduced airway hyperreactivity with a concomitant decrease in eosinophils in the lung as compared with control IgG-treated mice. Treatment with anti-B7-H3 mAb also resulted in decreased production of Th2 cytokines (IL-4, IL-5, and IL-13) in the draining lymph node cells. Although blockade of B7-H3 during the induction phase abrogated the development of asthmatic responses, B7-H3 blockade during the effector phase did not inhibit asthmatic responses. These results indicated an important role for B7-H3 in the development of pathogenic Th2 cells during the induction phase in a murine model of asthma.
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页码:4062 / 4071
页数:10
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