Hoffman R, Kopel S, Hsu S D, Dainiak N, Zanjani E D
Blood. 1978 Jul;52(1):255-60.
The pathogenesis of the anemia associated with malignancy was investigated in a patient with T cell chronic lymphocytic leukemia. The plasma clot culture system was used as a measure in vitro of erythropoiesis. The patient's peripheral blood and marrow T lymphocytes obtained both before and after transfusion therapy suppressed erythroid colony formation by normal human bone marrow cells. Pretreatment of the patient's bone marrow T cells by antithymocyte globulin (ATG) and complement reversed this suppression. In addition, pretreatment of the patient's marrow cells with ATG and complement markedly augmented erythropoiesis in vitro. The expression of erythroid activity caused by the selective destruction of the suppressor T lymphocytes in the patient's bone marrow with ATG and the suppression of normal erythropoiesis by the patient's bone marrow and peripheral blood lymphocytes suggest that interaction between the malignant T cell and the erythropoietin-responsive stem cell is important in production of anemia in this patient.
在一名T细胞慢性淋巴细胞白血病患者中,对与恶性肿瘤相关的贫血的发病机制进行了研究。血浆凝块培养系统被用作体外红细胞生成的一种测量方法。该患者在输血治疗前后获得的外周血和骨髓T淋巴细胞抑制了正常人骨髓细胞的红系集落形成。用抗胸腺细胞球蛋白(ATG)和补体对患者的骨髓T细胞进行预处理可逆转这种抑制作用。此外,用ATG和补体对患者的骨髓细胞进行预处理可显著增强体外红细胞生成。用ATG选择性破坏患者骨髓中的抑制性T淋巴细胞所引起的红系活性表达,以及患者的骨髓和外周血淋巴细胞对正常红细胞生成的抑制,表明恶性T细胞与促红细胞生成素反应性干细胞之间的相互作用在该患者贫血的发生中起重要作用。