期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 20, 页码 7409-7414出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1401662111
关键词
immunosuppression; LCMV
资金
- National Institutes of Health [AI085043, AI082975]
- Microbial Pathogenesis Training Grant [T32-AI07323]
- Virology and Gene Therapy Training Grant [T32AI060567]
- Fonds de la Recherche en Sante du Quebec
- Stein Oppenheimer Endowment Award
- University of California, Los Angeles (UCLA), Clinical and Translational Science Institute [UL1TR000124]
- UCLA Center for AIDS Research [P30 AI028697]
CD4 T cells are central to orchestrate, sustain, and potentially regenerate antiviral immunity throughout persistent viral infections. Although the evolving immune environment during persistent infection reshapes established CD4 T-cell responses, the fate of naive CD4 T cells primed in the midst of persistent infection is unclear. We demonstrate that, in marked contrast to the onset of infection, virus-specific CD4 T cells primed during an established persistent infection have diminished ability to develop Th1 responses, to efficiently accumulate in peripheral tissues, and almost exclusively differentiate into T follicular helper cells. Consistent with suppressed Th1 and heightened Tfh differentiation, virus-specific CD4 T cells primed during the established persistent infection provide help to B cells, but only limited help to CD8 T cells. The suppression of de novo Th1 generation and tissue distribution was mediated by chronic type I IFN (IFN-I) production and was effectively restored by blocking IFN-I signaling during CD4 T-cell priming. Thus, we establish a suppressive function of chronic IFN-I signaling and mechanism of immunoregulation during an established persistent virus infection.
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