[Effect of CD8+ effector T cells on the hematopoiesis pathway damage in the patients with severe aplastic anemia]

To investigate the quantity and the pathway to damage hematopoietic cells of CD8+CD25+ and CD8+ HLA-DR+ effector T cells in peripheral blood (PB) of severe aplastic anemia(SAA) patients and explore the immunopathogenesis of SAA.

The quantity of CD8+ CD25+ and CD8+ HLA-DR+ cells in PB and the expressions of perforin, granzyme B, tumor necrosis factor-beta (TNF-beta) and FasL in 29 SAA (14 untreated and 15 recovered) patients and 12 normal controls were analyzed by flow cytometry.

The fraction of CD8+ CD25+ T cells in CD8+ T cells was (3.67 +/- 2.58)% in untreated SAA patients, (5.19 +/- 4. 29)% in recovered patients and (4.84 +/- 2.31)% in normal controls, and that of CD8+ CD25+ T cells in CD3+ cells in the three groups was (2.25 +/- 1.35)%, (2.98 +/- 1.35)% and (2.11 +/- 1.88)%, respectively. They had no statistic difference among the 3 groups (P >0.05). The fraction of CD8+ HLA-DR+ T cells in CD8+ T cells was (39.30 +/- 8.13)% in untreated patients, which was significantly higher than that in recovered patients [(20.65 +/- 5.38)%] and controls [(18.34 +/- 6.68)%] (P<0.001), while there was no statistic difference between the latter two groups (P>0.05). CD8+ HLA-DR+ T cells in CD3+ cells was (27.81 +/- 7.10)% in untreated group, which was significantly higher than that of recovered group [(12.02 +/- 3.03)%] and controls [(8.50 +/-2.33)%] (P<0.01). And that in recovered group was higher than that in control group (P<0.05). The expressions of perforin, granzyme B, TNF-beta and FasL of CD8+ HLA-DR+ T cells in untreated group were 8.51%, 96.08%, 72.11% and 94.25% respectively, which were higher than those in recovered group (1.78%, 85.20%, 34.38% and 51.20%) and controls (1.86%, 82.09% ,17.92% and 32.91%). There was no statistic difference between recovered patients and controls (P>0.05).

There were elevated quantity of CD8+ HLA-DR+ T cells and high expressions of perforin, granzyme B, TNF-beta and FasL in SAA, which might contribute to the bone marrow failure.