Abstract
It has been emphasized that chronic generalized immune dysfunction is the leading event in the pathogenesis of HIV infection, in which the contribution of dendritic cells (DCs) and regulatory T cells (Tregs) should not be underestimated. In current study, we assessed the longitudinal changes of peripheral blood DC subsets and Tregs in chronically asymptomatic treatment-naive HIV-1-infected patients during 60 weeks of antiretroviral therapy (ART), and compared with those in healthy controls and long term non-progressors (LTNPs). Blood samples were collected at week 0, 4, 12, 24, 48 and 60 of treatment to measure the counts of DC subsets and Tregs by flow cytometry and IFN-a plasma levels by ELISA. The counts of myeloid dendritic cells (mDCs) increased during ART, reaching similar levels to healthy controls at week 60 post ART but still lower than those of LTNPs. In HIV-1-infected patients, the mDCs counts were directly correlated with CD4 counts during ART. Changes in mDCs at week 8 were positively correlated with the changes in CD4 counts at week 60 post ART. However, the counts and function of plasmacytoid dendritic cells (pDCs) remained relatively stable during ART, and similar to those in healthy controls and LTNPs. The percentage of Tregs increased before ART and normalized after ART. Importantly, we found pDCs counts were associated with percentage of Tregs during ART, which may help in understanding of the role of these cells in HIV infection.
Highlights
HIV infection is characterized with an initial, occasionally symptomatic acute phase followed by an asymptomatic period of variable length culminating in clinically evident immunodeficiency [1]
PDCs counts were positively associated with Tregs percentage (r = 0.343, p,0.001), but there were no correlations between myeloid dendritic cells (mDCs) counts and Tregs percentage (r = 0.181, p = 0.055)
HIV-1 RNA viral loads (VLs) and CD4 counts were measured in all 17 HIV-1-infected patients at week 0, 4, 8, 12, 24, 48 and 60 of antiretroviral therapy (ART) (Table 1)
Summary
HIV infection is characterized with an initial, occasionally symptomatic acute phase followed by an asymptomatic period of variable length culminating in clinically evident immunodeficiency [1]. Recent findings have emphasized that chronic generalized immune dysfunction is the leading event in the pathogenesis of HIV infection, in which the contribution of dendritic cells (DCs) and regulatory T cells (Tregs) should not be underestimated. DCs are professional antigen-presenting cells required for generation of adaptive immunity [2], and Tregs are essential for immune nullipotency and immune suppression via cell-cell contacts or cytokine secretion [3]. There are accumulating evidences that DCs and Tregs may be valuable tools for modulating immunity in the setting of chronic viral infections, and interactions between them may play a crucial role in the balance of immunity and tolerance. DCs are at the interface of innate and adaptive immunity, which specialize in the initiation of adaptive immune responses to invading pathogens such as HIV [4]. Two main subsets have been identified according to their different phenotypes and functions: myeloid and plasmacytoid DCs [5]
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