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Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease.

Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Research Abstract Details 

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  • Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Abstract Text:

    kevin sheKevin She,andrew l gilmanAndrew L Gilman,soudabeh aslanianSoudabeh Aslanian,hiromi shimizuHiromi Shimizu,mark krailoMark Krailo,zhengjia chenZhengjia Chen,gregor s reidGregor S Reid,donna wallDonna Wall,fred goldmanFred Goldman,kirk r schultzKirk R Schultz,

    B cells appear to play a role in chronic graft-versus-host disease (cGVHD) as shown in murine models and the success of anti-CD20 B cell antibody treatment in humans. Recent studies have shown that immunostimulatory microbial CpG-DNA splenic responses were enhanced in murine GVHD. We hypothesized that CpG-induced B cell responses are increased in human cGVHD. Newly diagnosed cGVHD patients enrolled on the COG protocol ASCT0031 were divided into early (3-8 months postblood and marrow transplant [BMT]) and late (> or =9 months post-BMT) onset groups and compared to time-matched control BMT patients. A significantly greater percentage of phosphorothioate (PS)-modified CpG stimulated B cells from cGVHD patients demonstrated an increased expression of CD86 compared to controls (P = .0004). This response had a significant correlation between B cell TLR9 expression (r(2) = 0.65; P = .002) and CD86 upregulation using the entirely TLR9-dependent native phosphodiester CpG (P = .003). The PS-modified CpG response at 2 months after initiation of cGVHD therapy demonstrated a trend toward predicting therapeutic response at 9 months post-BMT (P = .07). These findings suggest that an increased number of B cells, primed for a TLR9 response, may play a role in the pathophysiology of cGVHD.

    Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Publishing Authors By Initials

    k sheK She,al gilmanAL Gilman,s aslanianS Aslanian,h shimizuH Shimizu,m krailoM Krailo,z chenZ Chen,gs reidGS Reid,d wallD Wall,f goldmanF Goldman,kr schultzKR Schultz,

    For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

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    Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Biology of blood and marrow transplantation : jour

    VOLUME: 13

    Page Numbers: 386-97

    Journal Abbreviation: Biol. Blood Marrow Transplant.

    ISSN: 1083-8791

    DAY: 15

    MONTH: 02

    YEAR: 2007

    Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9600628

    Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Keywords Mesh Terms:

    KEYWORDS: Up-Regulation

    MESH TERMS: blood

    Chemical & Substance for Abstract: Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease. Information

    Substance Name: Toll-Like Receptor 9

    Registry Number: 0

    Grant and Affiliation Information for Altered Toll-like receptor 9 responses in circulating B cells at the onset of extensive chronic graft-versus-host disease.

    AFFILIATION: Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: CA 84137

    ACRONYM: CA

    MEDLINETA: Biol Blood Marrow Transplant

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    ACCESSION NUMBER:

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