About: Recent evidence has suggested that IL-10-producing effector CD8(+) T cells play an important role in regulating excessive inflammation during acute viral infections. However, the cellular and molecular cues regulating the development of IL-10-producing effector CD8(+) T cells are not completely defined. Here we show that type I interferons (IFNs) are required for the development of IL-10-producing effector CD8(+) T cells during influenza virus infection. We find that type I IFNs can enhance IL-27 production by lung antigen presenting cells, thereby facilitating IL-10-producing CD8(+) T cell development through a CD8(+) T cell non-autonomous way. Surprisingly, we also demonstrate that direct type I IFN signaling in CD8(+) T cells is required for the maximal generation of IL-10-producing CD8(+) T cells. Type I IFN signaling in CD8(+) T cells, in cooperation with IL-27 and IL-2 signaling, promotes and sustains the expression of IRF4 and Blimp-1, two transcription factors required for the production of IL-10 by effector CD8(+) T cells. Our data have revealed a critical role of the innate antiviral effector cytokines in regulating the production of a regulatory cytokine by effector CD8(+) T cells during respiratory virus infection. The potential implications of these findings for influenza virus infection are also discussed.   Goto Sponge  NotDistinct  Permalink

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  • Recent evidence has suggested that IL-10-producing effector CD8(+) T cells play an important role in regulating excessive inflammation during acute viral infections. However, the cellular and molecular cues regulating the development of IL-10-producing effector CD8(+) T cells are not completely defined. Here we show that type I interferons (IFNs) are required for the development of IL-10-producing effector CD8(+) T cells during influenza virus infection. We find that type I IFNs can enhance IL-27 production by lung antigen presenting cells, thereby facilitating IL-10-producing CD8(+) T cell development through a CD8(+) T cell non-autonomous way. Surprisingly, we also demonstrate that direct type I IFN signaling in CD8(+) T cells is required for the maximal generation of IL-10-producing CD8(+) T cells. Type I IFN signaling in CD8(+) T cells, in cooperation with IL-27 and IL-2 signaling, promotes and sustains the expression of IRF4 and Blimp-1, two transcription factors required for the production of IL-10 by effector CD8(+) T cells. Our data have revealed a critical role of the innate antiviral effector cytokines in regulating the production of a regulatory cytokine by effector CD8(+) T cells during respiratory virus infection. The potential implications of these findings for influenza virus infection are also discussed.
subject
  • Virology
  • Immunology
  • T cells
  • Immunostimulants
  • Interleukins
  • Biology terminology
  • Human cells
  • Companies of Tajikistan
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