File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Reduced incidence and severity of antigen-induced autoimmune diseases in mice lacking interferon regulatory factor-1

TitleReduced incidence and severity of antigen-induced autoimmune diseases in mice lacking interferon regulatory factor-1
Authors
Issue Date1997
Citation
Journal of Experimental Medicine, 1997, v. 185, n. 2, p. 231-238 How to Cite?
AbstractInterferon 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-1β-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)-γ 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.
Persistent Identifierhttp://hdl.handle.net/10722/291421
ISSN
2023 Impact Factor: 12.6
2023 SCImago Journal Rankings: 6.838
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTada, Yoshifumi-
dc.contributor.authorHo, Alexandra-
dc.contributor.authorMatsuyama, Toshifumi-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:20Z-
dc.date.available2020-11-17T14:54:20Z-
dc.date.issued1997-
dc.identifier.citationJournal of Experimental Medicine, 1997, v. 185, n. 2, p. 231-238-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/291421-
dc.description.abstractInterferon 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-1β-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)-γ 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.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleReduced incidence and severity of antigen-induced autoimmune diseases in mice lacking interferon regulatory factor-1-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1084/jem.185.2.231-
dc.identifier.pmid9016872-
dc.identifier.pmcidPMC2196116-
dc.identifier.scopuseid_2-s2.0-0031048823-
dc.identifier.volume185-
dc.identifier.issue2-
dc.identifier.spage231-
dc.identifier.epage238-
dc.identifier.isiWOS:A1997WE64400006-
dc.identifier.issnl0022-1007-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats