Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs.

Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Research Abstract Details 

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Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Abstract Text:

Anna Yarilina,Edward DiCarlo,Lionel B Ivashkiv,

Innate immune receptors that recognize nucleic acids, such as TLRs and RNA helicases, are potent activators of innate immunity that have been implicated in the induction and exacerbation of autoimmunity and inflammatory arthritis. Polyriboinosine-polyribocytidylic acid sodium salt (poly(IC)) is a mimic of dsRNA and viral infection that activates TLR3 and the RNA helicases retinoic acid-induced gene-1 and melanoma differentiation-associated gene-5, and strongly induces type I IFN production. We analyzed the effects of systemic delivery of poly(IC) on the inflammatory effector phase of arthritis using the collagen Ab-induced and KRN TCR-transgenic mouse serum-induced models of immune complex-mediated experimental arthritis. Surprisingly, poly(IC) suppressed arthritis, and suppression was dependent on type I IFNs that inhibited synovial cell proliferation and inflammatory cytokine production. Administration of exogenous type I IFNs was sufficient to suppress arthritis. These results suggest a regulatory role for innate immune receptors for dsRNA in modulating inflammatory arthritis and provide additional support for an anti-inflammatory function of type I IFNs in arthritis that directly contrasts with a pathogenic role in promoting autoimmunity in systemic lupus.

Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Publishing Authors By Initials

A Yarilina,E DiCarlo,LB Ivashkiv,

For similar virus diseases research abstracts see: virus diseases research

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Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 178

Page Numbers: 2204-11

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 15

MONTH: Feb

YEAR: 2007

Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Keywords Mesh Terms:

KEYWORDS: Virus Diseases

MESH TERMS: pathology

Chemical & Substance for Abstract: Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs. Information

Substance Name: RNA Helicases

Registry Number: EC 2.7.7.-

Grant and Affiliation Information for Suppression of the effector phase of inflammatory arthritis by double-stranded RNA is mediated by type I IFNs.

AFFILIATION: Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY 10021, USA.

Country: United States

AGENCY: United States NCRR

GRANT: C06-RR12538-01

ACRONYM: RR

MEDLINETA: J Immunol

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