中文摘要：

目的观察重型再生障碍性贫血（SAA）患者外周血CD8＋HLA—DR＋T淋巴细胞效应因子水平，进一步探讨SAA的免疫发病机制。方法采用免疫磁珠分选24例SAA初治患者及23名健康对照外周血CD8＋HIJA-DR＋效应T细胞，半定量反转录PCR检测分选细胞穿孔素、颗粒酶B、Fas配体（FasL）、肿瘤坏死因子β（TNF-β）mRNA表达情况。结果SAA初治组CD8＋HLA－DR＋效应T细胞的穿孔素、颗粒酶B、FasL、TNF－βmRNA的表达量分别为0．66±0．25、0．56±0．26、0．77±0．24、0．58±0．16，均明显高于健康对照（0．53±0．14、0．40±0．13、0．61±0．16、0．46±0．15，P=0．042、0．012、0．011、0．011）。结论CD8＋HIA—DR＋效应T细胞可能通过穿孔素、颗粒酶B途径、Fas／FasL途径及TNF-B途径损伤SAA患者骨髓造血细胞，在SAA免疫发病过程中发挥了重要作用。

英文摘要：

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 I＋ （TNF-13） 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-[3 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.