Turkish Journal of Hematology (Jul 2015)
Detection and Significance of CD4+CD25+CD127dim Regulatory T Cells in Individuals with Severe Aplastic Anemia
Abstract
INTRODUCTION: To investigate the relationship between CD4+CD25+CD127dim regulatory T cells (Tregs) and immune imbalance in acquired severe aplastic anemia (SAA). METHODS: The quantity of CD4+CD25+CD127dim 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+CD127dim 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+CD127dim 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+CD127dim 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+CD127dim Tregs/PBL and granulocyte counts and RET% (r=0.739, 0.749 respectively, p<0.01). DISCUSSION AND CONCLUSION: The decrease of CD4+CD25+CD127dim Tregs in SAA patients may cause excessive functions of T lymphocytes and thus lead to hematopoiesis failure in SAA.
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