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The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates.

The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Research Abstract Details 

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  • The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Abstract Text:

    aftab a ansariAftab A Ansari,lara e pereiraLara E Pereira,ann e mayneAnn E Mayne,nattawat onlamoonNattawat Onlamoon,kovit pattanapanyasatKovit Pattanapanyasat,kazuyasu moriKazuyasu Mori,f villingerF Villinger,

    Autoantibodies appear in the sera of rhesus macaques following SIV infection. The present study was conducted to examine the role of viral load, antiviral chemotherapy and stage of disease on the titers of such autoantibodies and the spectrum of autoantigens that become the target of such autoimmune responses. In addition, the role of regulatory T cells (Tregs) was also examined. Results of these studies showed that the highest autoantibody titers were noted in animals with lower relative plasma viral loads with a wider spectrum of autoantigens that are the target of such responses as compared with lower autoantibody titers in animals with relatively higher plasma viral loads and a narrower spectrum of autoantigens. Short-term antiviral chemotherapy did not influence the titers of autoantibodies. While there was a gradual decrease in the frequency and absolute number of Tregs, the levels of Tregs was inversely correlated with viral load and lower autoantibody titers. The mechanisms for these differences remain unknown and suggest complex relationships exist between levels of immunosuppression, autoimmune response, homeostatic proliferation and the spectrum of autoantigens that become the target of such autoimmune responses.

    The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Publishing Authors By Initials

    aa ansariAA Ansari,le pereiraLE Pereira,ae mayneAE Mayne,n onlamoonN Onlamoon,k pattanapanyasatK Pattanapanyasat,k moriK Mori,f villingerF Villinger,

    For similar investigative techniques: clinical laboratory techniques: microbiological techniques: viral load research abstracts see: investigative techniques: clinical laboratory techniques: microbiological techniques: viral load research

    PUBMED ID PMID:

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    The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Journal Published:

    PUBLICATION TYPE: Review

    Journal: Journal of autoimmunity

    VOLUME: 28

    Page Numbers: 152-9

    Journal Abbreviation:

    ISSN: 0896-8411

    DAY: 26

    MONTH: 03

    YEAR: 2007

    The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8812164

    The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Keywords Mesh Terms:

    KEYWORDS: Viral Load

    MESH TERMS: immunology

    Chemical & Substance for Abstract: The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Information

    Substance Name: Autoantigens

    Registry Number: 0

    Grant and Affiliation Information for The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates.

    AFFILIATION: Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. pathaaa@emory.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NCRR

    GRANT: R24 RR-16988

    ACRONYM: RR

    MEDLINETA: J Autoimmun

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    DATABASENAME:

    ACCESSION NUMBER:

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