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Content Provider | World Health Organization (WHO)-Global Index Medicus |
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Author | Srivastava, Shivani Koch, Lisa K. Campbell, Daniel J. |
Description | Author Affiliation: Srivastava S ( Immunology Program, Benaroya Research Institute, Seattle, WA 98101); Koch LK ( Immunology Program, Benaroya Research Institute, Seattle, WA 98101); Campbell DJ ( Immunology Program, Benaroya Research Institute, Seattle, WA 98101) |
Abstract | Type I IFNs are a family of proinflammatory cytokines that are essential for antiviral immunity but whose overexpression is associated with several autoimmune disorders. In this study, we asked how chronic IFN overexpression regulates the activity of different cell types and how this contributes to immune dysfunction during IFN-associated inflammatory diseases. We show that in mice that chronically overproduce type I IFNs owing to loss of the DNA exonuclease Trex1, inflammatory disease completely depends on IFN R signaling in T cells. Although IFNs directly inhibited the proliferation and activation of Foxp3(+) regulatory T cells, this was neither required nor sufficient for development of inflammatory disease. Rather, chronic IFN expression directly promoted the expansion and activation of effector T cells, and disease development was completely dependent on IFN R signaling in these cells. Thus, chronic IFN expression can drive inflammatory disease via its direct effects on effector, but not regulatory, T cells. |
ISSN | 00221767 |
e-ISSN | 15506606 |
DOI | 10.4049/jimmunol.1401039 |
Journal | The Journal of Immunology |
Issue Number | 6 |
Volume Number | 193 |
Language | English |
Publisher | The American Association of Immunologists |
Publisher Date | 2014-09-15 |
Publisher Place | United States |
Access Restriction | Open |
Subject Keyword | Colitis Immunology Inflammation Interferon Type I Receptor, Interferon Alpha-beta T-lymphocytes, Regulatory Animals Autoimmune Diseases Cell Proliferation Cells, Cultured Genetics Exodeoxyribonucleases Forkhead Transcription Factors Biosynthesis Lymphocyte Activation Mice Mice, Inbred C57bl Mice, Knockout Phosphoproteins Signal Transduction Research Support, N.i.h., Extramural Discipline Immunology |
Content Type | Text |
Resource Type | Article |
Subject | Immunology and Allergy Immunology |
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