Talay Oezcan, Shen Ching-Hung, Chen Lieping, Chen Jianzhu
Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2741-6. doi: 10.1073/pnas.0813367106. Epub 2009 Feb 6.
Studies have shown that T-cell-dendritic cell (DC) interaction is required for efficient DC maturation. However, the identities of the molecules that mediate the interaction in vivo are largely unknown. Here, we show that maturation of DCs as well as CD8 T-cell responses were impaired in B7-H1-deficient (B7-H1(-/-)) mice to influenza virus infection. Both defects were restored by transferring B7-H1-expressing naïve T cells into B7-H1(-/-) mice. Similarly, transferring DCs from wild-type mice or from RAG1(-/-) mice that had been injected with B7-H1-expressing naïve T cells also restored CD8 T-cell responses in B7-H1(-/-) mice. These results demonstrate that B7-H1 on naïve T cells is required to condition immature DCs to undergo efficient maturation when they encounter microbial infection. In return, the mature DCs stimulate a robust T-cell response against the infecting pathogen.
研究表明,有效的树突状细胞(DC)成熟需要T细胞与DC的相互作用。然而,介导体内这种相互作用的分子身份在很大程度上尚不清楚。在此,我们发现,在缺乏B7-H1(B7-H1(-/-))的小鼠中,DC的成熟以及CD8 T细胞反应在流感病毒感染时受损。通过将表达B7-H1的幼稚T细胞转移到B7-H1(-/-)小鼠中,这两种缺陷均得到恢复。同样,将来自野生型小鼠或已注射表达B7-H1的幼稚T细胞的RAG1(-/-)小鼠的DC转移到B7-H1(-/-)小鼠中,也能恢复CD8 T细胞反应。这些结果表明,幼稚T细胞上的B7-H1是使未成熟DC在遇到微生物感染时能够有效成熟所必需的。反过来,成熟的DC会刺激针对感染病原体的强大T细胞反应。