Journal article
TRAF3 enhances type I interferon receptor signaling in T cells by modulating the phosphatase PTPN22
Science signaling, Vol.15(753), pp.eabn5507-eabn5507
09/27/2022
DOI: 10.1126/scisignal.abn5507
PMCID: PMC9728096
PMID: 36166512
Abstract
Running interference for interferon Type I interferons (IFNs) are antiviral cytokines produced by infected cells that stimulate an innate immune response through their receptors (IFNARs). Hornick et al. characterized the regulation of type I IFN signaling in CD4+ T cells in the adaptive immune system. Compared with wild-type cells, CD4+ T cells deficient in the adaptor protein TRAF3 showed reduced expression of IFN-responsive genes and reduced receptor-proximal signaling, including decreased activation of the transcriptional regulator STAT1. In the absence of TRAF3, the inhibitory phosphatase PTPN22 was recruited to the IFNAR complex, which blocked STAT1 activation. Treatment of TRAF3-deficient cells with a PTPN22 inhibitor restored their responsiveness to type I IFNs. Together, these data indicate that TRAF3 promotes T cell activation by type I IFNs by preventing the inhibition of receptor signaling.
Details
- Title: Subtitle
- TRAF3 enhances type I interferon receptor signaling in T cells by modulating the phosphatase PTPN22
- Creators
- Emma Hornick - University of IowaAlicia Wallis - University of IowaGail Bishop - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Science signaling, Vol.15(753), pp.eabn5507-eabn5507
- DOI
- 10.1126/scisignal.abn5507
- PMID
- 36166512
- PMCID
- PMC9728096
- NLM abbreviation
- Sci Signal
- ISSN
- 1945-0877
- eISSN
- 1937-9145
- Publisher
- The American Association for the Advancement of Science
- Language
- English
- Date published
- 09/27/2022
- Academic Unit
- Microbiology and Immunology; President; Fraternal Order of Eagles Diabetes Research Center
- Record Identifier
- 9984302599502771
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