Detection and Significance of CD4+CD25+CD127dim Regulatory T Cells in Individuals with Severe Aplastic Anemia.
Background: To investigate the relationship between CD4(+)CD25(+)CD127(dim) regulatory T cells (Tregs) and immune imbalance in acquired severe aplastic anemia (SAA).
Methods: The quantity of CD4(+)CD25(+)CD127(dim) Tregs in 44 SAA patients and 23 normal controls were measured by flow cytometry. Correlations between Tregs and T cell subsets, dendritic cell (DC) subsets, granulocyte counts and percentage of reticulocytes (RET%) were analyzed.
Results: The percentage of CD4(+)CD25(+)CD127(dim) Tregs in peripheral blood lymphocytes (PBL) of untreated patients was lower than in recovery patients and normal controls (0.83 ± 0.44% vs 2.91 ± 1.24% and 2.18 ± 0.55%, respectively, p<0.05). The percentage of CD4(+)CD25(+)CD127(dim) Tregs in CD4(+) T lymphocytes of recovery patients was higher than for untreated patients and normal controls (9.39 ± 3.51% vs 7.61 ± 5.3% and 6.83 ± 1.4%, respectively, p<0.05). The percentage of CD4(+) T lymphocytes in PBL of untreated patients was lower than for recovery patients and normal controls (13.55 ± 7.37% vs 31.82 ± 8.43% and 32.12 ± 5.88%, respectively, p<0.05). T cell subset (CD4(+)/CD8(+) ratio) was 0.41 ± 0.24 in untreated patients, which was lower than recovery patients (1.2 ± 0.4) and normal controls (1.11 ± 0.23) (p<0.05). DC subset (myeloid DC/plasmacytoid DC ratio, DC1/DC2 ratio) was 3.08 ± 0.72 in untreated patients, which was higher than recovery patients (1.61 ± 0.49) and normal controls (1.39 ± 0.36) (p<0.05). The percentage of CD4(+)CD25(+)CD127(dim) Tregs in PBL was positively associated with T cell subset (r=0.955, p<0.01), and negatively associated with DC subset (r=-0.765, p<0.01). There were significant positive correlations between CD4(+)CD25(+)CD127(dim) Tregs/PBL and granulocyte counts and RET% (r=0.739, 0.749 respectively, p<0.01).
Conclusions: The decrease of CD4(+)CD25(+)CD127(dim) Tregs in SAA patients may cause excessive functions of T lymphocytes and thus lead to hematopoiesis failure in SAA.