Tohda S, Suzuki T, Nagata K, Nara N, Aoki N
First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Nihon Ketsueki Gakkai Zasshi. 1990 Feb;53(1):14-20.
To determine the mechanism by which haematopoiesis is suppressed in aplastic anaemia, the effect of the sera from 6 patients on the granulopoietic precursors (colony-forming units in culture; CFU-C) was studied in vitro. Addition of the sera from 2 patients significantly suppressed CFU-C. The suppressive effect of the sera on CFU-C was inhibited by the addition of 1.5 NU/ml of anti-gamma-IFN antibody. In another patient, anti-gamma-IFN antibody increased autologous CFU-C although the serum of the patient did not suppress CFU-C. Serum gamma-IFN levels of all patients were under 2 IU/ml. The above findings suggest that humoral factors inhibit haematopoiesis in some patients with aplastic anaemia, and that gamma-IFN plays a role as an inhibitor even at a low concentration.
为了确定再生障碍性贫血中造血功能被抑制的机制，我们在体外研究了6例患者的血清对粒细胞生成前体细胞（培养中的集落形成单位；CFU-C）的影响。添加2例患者的血清可显著抑制CFU-C。添加1.5 NU/ml的抗γ-干扰素抗体可抑制血清对CFU-C的抑制作用。在另一例患者中，尽管该患者的血清未抑制CFU-C，但抗γ-干扰素抗体增加了自体CFU-C。所有患者的血清γ-干扰素水平均低于2 IU/ml。上述发现表明，体液因子在某些再生障碍性贫血患者中抑制造血功能，并且γ-干扰素即使在低浓度下也作为一种抑制剂发挥作用。
