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Eur J Immunol. 2016 Oct 4. doi: 10.1002/eji.201646548. [Epub ahead of print]
Type I IFN signaling facilitates the development of IL-10-producing effector CD8+ T cells during murine influenza virus infection.
Jiang L1,2, Yao S1,2, Huang S1,2, Wright J3, Braciale TJ3, Sun J4,5.
Author information
Abstract
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 in mice. 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 reveal 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. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
CD8+ T cells; IL-10; IL-27; Influenza; Type I IFN
PMID: 27701741 DOI: 10.1002/eji.201646548
[PubMed - as supplied by publisher]
Type I IFN signaling facilitates the development of IL-10-producing effector CD8+ T cells during murine influenza virus infection.
Jiang L1,2, Yao S1,2, Huang S1,2, Wright J3, Braciale TJ3, Sun J4,5.
Author information
Abstract
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 in mice. 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 reveal 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. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
CD8+ T cells; IL-10; IL-27; Influenza; Type I IFN
PMID: 27701741 DOI: 10.1002/eji.201646548
[PubMed - as supplied by publisher]