CD4+ T cell count and CD8+CD38+ cells were also significantly associated with the absolute count of Tregs. Univariate regression output results are displayed in Table 3. Multivariate least-square regression analysis was used to test the strength of the predictive ability of the parameters on the proportion and absolute MI-503 cost count of Tregs. When using the proportion of Tregs as the dependent variable, viral load was a statistically significant predictor (P < 0.001). Every unit increase in the proportion of Tregs corresponded to a 0.52 unit increase in viral load (measured in log copies per μL of blood). Using the absolute number of Tregs as the dependent
variable, multivariate regression showed that CD4+ T cell counts and viral load were both positively associated with the dependent variable (both P < 0.01), with every unit increase in the absolute count of Tregs corresponding to a 0.496 unit increase in viral load and a 0.776 unit increase in CD4+ T cell count. Multivariate regression output results are displayed in Table 4. The expression of CTLA-4 is associated with suppressive Treg cell function. This study found that HIV-infected slow progressors had lower CTLA-4 levels (27.7% positive) than asymptomatic HIV-infected patients (36.9%) and AIDS patients (40.6%), and were comparable to normal controls (23.8%,
Fig. 3). The level of the expression of CTLA-4 within Tregs was inversely correlated with CD4+ T cell count PF-01367338 (r=−0.419, P < 0.05), but had no relationship with the viral load in HIV-infected patients. Depletion of CD25+ cells augments the IFN-γ expression in CD8+ T cells stimulated by HIV Gag peptide mix in both HIV-infected SPs and asymptomatic HIV patients. The suppressive activity of Tregs in HIV-infected SPs, as measured by the relative inhibition of IFN-γ expression stimulated by HIV Gag peptide mix, was not significantly
different from that in asymptomatic HIV-infected patients (Fig. 4). It has been reported that peripheral Treg levels are closely Tacrolimus (FK506) associated with patterns of HIV disease progression (11, 13); however, the nature and role of Tregs in HIV disease progression is still a matter of debate (4, 5, 7, 10–15). As a cell expressing the CD4 receptor, Treg cells are vulnerable to entry by HIV, leading to progressive reduction in their absolute numbers over the course of HIV infection (15). Previous research suggests that HIV may selectively promote Treg survival via a CD4-gp120-dependent pathway (13), and high levels of immune activation in immunodeficient patients might induce and maintain a population of Tregs as a negative feedback (15). Our present data showed that SPs had the highest absolute number of Tregs and the lowest proportion of Tregs in peripheral blood as compared to asymptomatic HIV-infected patients and AIDS patients, with the proportion of Tregs increasing as the CD4+ T cell count fell.