Dallalio G, North M, Means R T
Hematology/Oncology Division, University of Cincinnati College of Medicine, Ohio, USA.
Am J Hematol. 1996 Oct;53(2):118-20. doi: 10.1002/(SICI)1096-8652(199610)53:2<118::AID-AJH10>3.0.CO;2-B.
Increased production of cytokines such as beta-interferon (IFN) and gamma-IFN may contribute to the anemia frequently observed in patients with human immunodeficiency virus (HIV) infection. The hypothesis that HIV infection might enhance the susceptibility of erythroid progenitors to cytokine-mediated inhibition was evaluated by comparing the effects of beta- and gamma-IFN on in vitro colony formation by marrow erythroid colony-forming units (CFU-E) from HIV patients, normal volunteers, and anemic non-HIV-infected individuals. CFU-E colony formation from HIV patients was not significantly different from controls, and the degree of inhibition by IFN did not differ among patient subsets. HIV infection does not appear to impair baseline CFU-E colony formation, nor does it appear to enhance the susceptibility of CFU-E to suppression by cytokines.
诸如β-干扰素（IFN）和γ-干扰素等细胞因子产量的增加，可能是导致人类免疫缺陷病毒（HIV）感染患者中常见贫血的原因之一。通过比较β-干扰素和γ-干扰素对来自HIV患者、正常志愿者以及贫血的非HIV感染个体的骨髓红系集落形成单位（CFU-E）体外集落形成的影响，对HIV感染可能会增强红系祖细胞对细胞因子介导抑制的易感性这一假说进行了评估。HIV患者的CFU-E集落形成与对照组无显著差异，并且各患者亚组中干扰素的抑制程度也无差异。HIV感染似乎不会损害基线CFU-E集落形成，也不会增强CFU-E对细胞因子抑制作用的易感性。
