Expression of B7-H1 and B7-DC on the airway epithelium is enhanced by double-stranded RNA

被引:35
|
作者
Tsuda, M
Matsumoto, K
Inoue, H [1 ]
Matsumura, M
Nakano, T
Mori, A
Azuma, M
Nakanishi, Y
机构
[1] Kyushu Univ, Grad Sch Med Sci, Res Inst Dis Chest, Higashi Ku, Fukuoka 8128582, Japan
[2] Natl Hosp Organizat Sagamihara Natl Hosp, Clin Res Ctr Allergy & Rheumatol, Sagamihara, Kanagawa 2288522, Japan
[3] Tokyo Med & Dent Univ, Dept Mol Immunol, Grad Sch, Bunkyo Ku, Tokyo, Japan
关键词
innate immunity; double-stranded RNA; IFN-gamma; IL-13; programmed death-1; BEAS-2B; T cell clone; glucocorticoid;
D O I
10.1016/j.bbrc.2005.02.161
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Viral infection in the airway provokes various immune responses, including Th1 and Th2 responses, which are partly initiated by double-stranded RNA (dsRNA), a viral product for its replication. B7-H1 (PD-L1) and B7-DC (PD-L2) are B7-family molecules that bind to programmed death-1 (PD-1) on lymphocytes and are implicated in peripheral tolerance. We investigated the effect of dsRNA on the expression of B7-H1 and B7-DC on airway epithelial cell lines. B7-H1 and B7-DC were constitutively expressed on the cells, and their expression was profoundly upregulated by stimulation with an analog of viral dsRNA, polyinosinic-polycytidylic acid. B7-H1 and B7-DC were also upregulated by stimulation with IFN-gamma, IL-13, and the supernatant from T cell clones. A relatively high concentration of dexamethasone (1 mu M) was required to suppress the upregulation of B7-H1 or B7-DC. These results suggest that epithelial B7-H1 and B7-DC play a role in virus-associated immune responses in the airways. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:263 / 270
页数:8
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