Publication: The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates
1
Issued Date
2007-03-01
Resource Type
ISSN
10959157
08968411
08968411
Other identifier(s)
2-s2.0-34247629362
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Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Autoimmunity. Vol.28, No.2-3 (2007), 152-159
Suggested Citation
Aftab A. Ansari, Lara E. Pereira, Ann E. Mayne, Nattawat Onlamoon, Kovit Pattanapanyasat, Kazuyasu Mori, F. Villinger The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates. Journal of Autoimmunity. Vol.28, No.2-3 (2007), 152-159. doi:10.1016/j.jaut.2007.02.014 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/24575
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Title
The role of disease stage, plasma viral load and regulatory T cells (Tregs) on autoantibody production in SIV-infected non-human primates
Abstract
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. © 2007 Elsevier Ltd. All rights reserved.