Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 206, Issue 8, Pages 1647-1651Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20091507
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Funding
- Intramural NIH HHS Funding Source: Medline
- NIAID NIH HHS [HHSN266200700010C, R01AI46954, P01 AI082325, U19AI083025, U54 AI057158, U19 AI083025, U01AI070469, P01AI082325, R01 AI046954, P01AI058113, U01 AI070469, P01 AI058113] Funding Source: Medline
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Dysregulated innate responses, particularly excessive activation of interferon (IFN) pathways, have been implicated in the development of autoimmune pathologies. Autoreactivity frequently targets IFN-inducible genes such as the Ro autoantigens, which ubiquitinate and inhibit interferon regulatory factors (IRFs). A new study validates the role of these common autoantigens in preventing autoimmunity. The findings reveal that injury-induced systemic autoimmune disease is exacerbated in the absence of Ro52/Trim21 and is driven by the IL-23-Th17 pathway.
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