Expression of B7-H1 and B7-DC on the airway epithelium is enhanced by double-stranded RNA |
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Authors: | Tsuda Miyuki Matsumoto Koichiro Inoue Hiromasa Matsumura Mikiko Nakano Takako Mori Akio Azuma Miyuki Nakanishi Yoichi |
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Institution: | Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. |
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Abstract: | 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 microM) 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. |
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Keywords: | Innate immunity Double-stranded RNA IFN-γ IL-13 Programmed death-1 BEAS-2B T cell clone Glucocorticoid |
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