OBJECTIVE: To examine the expression of lymphokines damaging hematopoietic cells by CD8(+)HLA-DR(+) effector T cells in peripheral blood (PB) of the patients with severe aplastic anemia (SAA) and explore further the heterogeneous immunopathogenesis of SAA. METHODS: The CD8(+)HLA-DR(+) cells were sorted by immunomagnetic separation from the PB of 24 untreated SAA patients and 23 normal controls. The mRNA expressions of perforin, granzyme B, FasL and tumor necrosis factor β (TNF-β) of sorted cells were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The mRNA levels of perforin, granzyme B of CD8(+)HLA-DR(+)T cells in untreated group were higher than those of the controls (0.66 ± 0.25, 0.56 ± 0.26 vs 0.53 ± 0.14, 0.40 ± 0.13, P = 0.042, 0.012). The mRNA level of FasL in CD8(+)HLA-DR(+) T cells of untreated SAA patients was higher than that of the controls (0.77 ± 0.24 vs 0.61 ± 0.16, P = 0.011). The mRNA of TNF-β in CD8(+)HLA-DR(+) T cells of untreated SAA patients was also higher than that of the controls (0.58 ± 0.16 vs 0.46 ± 0.15, P = 0.011). CONCLUSIONS: CD8(+)HLA-DR(+) T cells may damage hematopoiesis through the actions of perforin, granzyme B, TNF-β and FasL. And it thus contributes to the immunopathogenesis of SAA.
OBJECTIVE: To examine the expression of lymphokines damaging hematopoietic cells by CD8(+)HLA-DR(+) effector T cells in peripheral blood (PB) of the patients with severe aplastic anemia (SAA) and explore further the heterogeneous immunopathogenesis of SAA. METHODS: The CD8(+)HLA-DR(+) cells were sorted by immunomagnetic separation from the PB of 24 untreated SAApatients and 23 normal controls. The mRNA expressions of perforin, granzyme B, FasL and tumor necrosis factor β (TNF-β) of sorted cells were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The mRNA levels of perforin, granzyme B of CD8(+)HLA-DR(+)T cells in untreated group were higher than those of the controls (0.66 ± 0.25, 0.56 ± 0.26 vs 0.53 ± 0.14, 0.40 ± 0.13, P = 0.042, 0.012). The mRNA level of FasL in CD8(+)HLA-DR(+) T cells of untreated SAApatients was higher than that of the controls (0.77 ± 0.24 vs 0.61 ± 0.16, P = 0.011). The mRNA of TNF-β in CD8(+)HLA-DR(+) T cells of untreated SAApatients was also higher than that of the controls (0.58 ± 0.16 vs 0.46 ± 0.15, P = 0.011). CONCLUSIONS:CD8(+)HLA-DR(+) T cells may damage hematopoiesis through the actions of perforin, granzyme B, TNF-β and FasL. And it thus contributes to the immunopathogenesis of SAA.