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Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Highly active antiretroviral therapy responders exhibit a phenotypic lymphocyte pattern comparable to that of
1Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, University of Vienna Medical School, Währinger Gürtel 18-20, A-1090 Vienna, Austria. sylvia.knapp@akh-wien.ac.at
Background:
The implementation of highly active antiretroviral therapy (HAART) in patients with progressive HIV-1 disease has resulted in a marked reduction of HIV-1-associated morbidity and mortality. In fact, the risk of HAART responders to develop opportunistic infections becomes similar to that of long-term nonprogressors (LTNPs).
Methods:
Reasoning that HAART may ultimately have consequences on both the quantity and quality of immune responses of a HIV-1-infected person, we assessed CD4+ and CD8+ T cell subsets in HAART recipients over a time period of 15 months and compared them to the lymphocyte phenotype of LTNPs and healthy controls. Evaluations included quantitative determinations of memory (CD45RO+CD62L-), naive (CD45RO-CD62L+), effector (CD27-, CD28-) and activated (HLA-DR+, CD38+, CD95+) CD4+ and CD8+ lymphocytes. The T cell function was assayed by skin tests.
Results:
Compared to healthy persons, treatment-naive patients with progressive disease exhibited a considerable reduction of CD4+ T cells with many of the remaining T cells showing signs of activation at baseline. CD8+ T cells were greatly increased in number, mainly because of an expansion of CD28- effector and memory CD8+ T cells. LTNPs, in contrast, had stable CD4+ and elevated CD8+ T cell counts, the latter being mainly due to a marked increase in CD27- effector cells. Essentially, the same immunophenotype was seen in HAART responders after 15 months of treatment when compared to LTNPs.
Conclusions:
It is tempting to speculate that a HAART-induced reduction in viral load may influence the immune system's capacity to mount protective responses to pathogenic microorganisms.
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