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By
From the Amgen Institute, Ontario Cancer Institute, and Departments of Medical Biophysics and
Immunology, University of Toronto, Toronto, Ontario, Canada M5G 2C1
Interferon regulatory factor-1 (IRF-1) is a transcription factor that regulates interferon-induced
genes and type I interferons. Recently, studies of IRF-1-deficient mice have revealed that
IRF-1 regulates the induction of molecules that play important roles in inflammation, such as
inducible nitric oxide synthase (iNOS) and interleukin-1
-converting enzyme (ICE). To study
the role of IRF-1 in autoimmunity, we investigated type II collagen-induced arthritis (CIA),
and experimental allergic encephalomyelitis (EAE), in mice lacking IRF-1. The incidence and
severity of CIA were significantly decreased in IRF-1
/ mice compared with IRF-1+/ mice,
as was the production of interferon (IFN)-
in lymph node cells. Both IRF-1+/ and IRF-1/
mice exhibited mild and transient disease after adoptive transfer of a type II collagen (CII)-specific T cell line together with sera from arthritic mice, but the IRF-1/ mice were less severely affected than the IRF-1+/ mice. In addition, the incidence of EAE in IRF-1/ mice
was decreased as compared with IRF-1+/ mice. Reverse transcription polymerase chain reaction showed that IRF-1 mRNA was constitutively expressed in the spinal cords of IRF-1+/
mice, and was upregulated in mice with clinical EAE. Expression of iNOS was also detected in
inflamed spinal cords. These results suggest that IRF-1 plays a key role in promoting inflammation and autoimmunity in CIA and EAE animal models.
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