Increased frequencies of CD57+ and
HLA-DR+ cell populations in CD4+ T
cell subsets in male homosexual HIV-1 infection
We next analyzed alterations in the expression of replicative senescence
and activation markers in the different CD4+ T cell
subsets. The results are presented in Table 2. For TN, the frequencies
of CD57+ cells were elevated within HIV-infected
patients (n = 30, 1.425 [0.905~3.968]%) compared to
healthy controls (n = 28, 0.95 [0.5425~1.728]%,p = 0.0297) (Fig. 2a). Similar expansion was observed in the TCM,
TEM, and TemRA subsets (p = 0.0041, 0.0032, and p< 0.0001, respectively) (Fig. 2c, e, and g). When we measured
the level of HLA-DR expression, we observed a similar expression pattern
compared to CD57 regarding elevated HLA-DR expression on all
CD4+ T cell subsets (Fig. 2b, d, f, h). Thus, a higher
percentage of CD57 and HLA-DR expression on CD4+ T
cell subsets was observed in HIV-infected patients compared to healthy
controls. This suggests accelerated immune senescence in HIV-infected
patients. On the other hand, the effects of ART on
CD4+ T cell surface senescence and activation markers
were also analyzed. When the frequencies of CD57+cells of the different CD4+ T cell subsets were
analyzed, we only observed a significant reduction on TemRA cells in
ART-receiving patients (n = 30, 61.85 [49.4~100]%)
compared to that of ART-naive subjects (n = 30, 76.80
[66.70~100]%, p = 0.0358) (Fig. 2g), but not
on TN, TCM, or TEM. Similar effects were observed for the frequencies of
HLA-DR+ cells of different CD4+ T
cell subsets, showing a significant decrease in frequencies of
HLR-DR+ cells on TCM, TEM, and TemRA compared to
ART-naive patients (p = 0.0006, 0.0269, and 0.0019, respectively)
(Fig. 2d, f, and h); however, there was no statistically significant
difference in TN.
Collectively, our data demonstrate increased frequencies of
CD57+ and HLA-DR+ cell populations
in most CD4+ T cell subsets in chronically
HIV-infected subjects, which can be partially reversed following ART.