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Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus.

Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Research Abstract Details 

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  • Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Abstract Text:

    zhongjie maZhongjie Ma,fangqi chenFangqi Chen,michael p madaioMichael P Madaio,philip l cohenPhilip L Cohen,robert a eisenbergRobert A Eisenberg,

    Chronic graft-vs-host (cGVH) disease is induced in nonautoimmune mice by the transfer of alloreactive T cells that recognize foreign MHC class II. It closely resembles systemic lupus erythematosus, with antinuclear Abs and immune-mediated nephritis. Recent work has implicated TLRs, particularly TLR9, in the recognition of certain autoantigens in vitro and in vivo. To explore further the role of TLR9 in systemic autoimmunity, we induced cGVH disease in C57BL/6 (B6) mice lacking TLR9, including B6 mice expressing the anti-DNA-encoding IgH transgenes 3H9 or 56R (B6.3H9.TLR9(-/-), B6.56R.TLR9(-/-)). We found that cGVH disease caused breakdown of B cell tolerance to chromatin and DNA in TLR9(-/-) recipients of alloreactive cells, yet that nephritis was less severe and that some autoantibody titers were lower compared with B6-cGVH controls. Spleen lymphocyte analysis showed that cGVH disease strikingly depleted marginal zone B cells in B6 mice, but did not influence T cell subsets in either B6 or B6-TLR9(-/-) hosts. B6.56R.TLR9(-/-) mice had less spontaneous production of autoantibodies than B6.56R mice, but there were no significant differences between B6.56R and B6.56R.TLR9(-/-) postinduction of cGVH disease. Taken together, these results suggested that TLR9 may worsen some aspects of systemic autoimmunity while alleviating others.

    Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Publishing Authors By Initials

    z maZ Ma,f chenF Chen,mp madaioMP Madaio,pl cohenPL Cohen,ra eisenbergRA Eisenberg,

    For similar proteins: dna-binding proteins: toll-like receptor 9 research abstracts see: proteins: dna-binding proteins: toll-like receptor 9 research

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    Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

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

    VOLUME: 177

    Page Numbers: 7444-50

    Journal Abbreviation: J. Immunol.

    ISSN: 0022-1767

    DAY: 15

    MONTH: Nov

    YEAR: 2006

    Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Keywords Mesh Terms:

    KEYWORDS: Toll-Like Receptor 9

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus. Information

    Substance Name: Rheumatoid Factor

    Registry Number: 9009-79-4

    Grant and Affiliation Information for Modulation of autoimmunity by TLR9 in the chronic graft-vs-host model of systemic lupus erythematosus.

    AFFILIATION: Division of Rheumatology, Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: U19-AI-46358

    ACRONYM: AI

    MEDLINETA: J Immunol

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