Detrick R A, Schulman J C, Mamus S W, McEver R P, Zanjani E D
Department of Medicine, Veterans Administration Medical Center, Minneapolis, MN.
Adv Exp Med Biol. 1988;241:199-215. doi: 10.1007/978-1-4684-5571-7_23.
T cells and monocytes/macrophages (Mo) have been shown to play important roles in modulating the growth and differentiation of human erythroid and myeloid progenitors and have been implicated in the mechanisms of gamma interferon (gamma-IFN) mediated suppression of normal human marrow erythroid progenitors in vitro. In order to assess the importance of T cells and Mo in the growth of human megakaryocytic progenitors (CFU-Mk) in vitro and to investigate gamma-IFN effect on human megakaryocytopoiesis, normal human marrow (BM) was cultured in plasma clot in the presence and absence T cells, Mo and gamma-IFN under conditions that support the formation of CFU-Mk derived colonies. The removal of T cells from BM (BM-T) caused a significant decrease (71.3 +/- 3.2 colonies observed vs 231.2 +/- 38.5 colonies predicted) in both the number and size of CFU-Mk derived colonies, and no such changes were seen with Mo depletion (BM-Mo); co-culture of autologous T cells with BM depleted of both Mo and T cells (BM-Mo-T) caused a significant increase in CFU-Mk derived colonies and restored colony size. The addition of gamma-IFN (less than 50-10,000 IU/ml) to BM caused a dose dependent inhibition of CFU-Mk (0-90%) as evidenced by decreased colony numbers and reduced colony size. The addition of gamma-IFN (50-10,000 IU/ml) to BM-T caused reduced inhibition of CFU-Mk (0-60%); co-culture of T cells (but not Mo) pre-incubated with gamma-IFN (10,000 IU/ml; 1 hour, 37 C followed by washing X 3) resulted in supression of CFU-Mk (80% inhibition with the addition of 1:4 T cells:marrow cells). The results demonstrate that T cells have the ability to modulate the growth of human CFU-Mk in vitro and may, under appropriate conditions, either promote (normal T cells) or inhibit (gamma-IFN activated T Cells) human megakaryocytopoiesis.
T细胞和单核细胞/巨噬细胞（Mo）已被证明在调节人类红系和髓系祖细胞的生长和分化中发挥重要作用，并且与γ干扰素（γ-IFN）介导的体外抑制正常人骨髓红系祖细胞的机制有关。为了评估T细胞和Mo在体外人巨核细胞祖细胞（CFU-Mk）生长中的重要性，并研究γ-IFN对人巨核细胞生成的影响，在支持CFU-Mk衍生集落形成的条件下，将正常人骨髓（BM）在有或无T细胞、Mo和γ-IFN的情况下于血浆凝块中培养。从BM中去除T细胞（BM-T）导致CFU-Mk衍生集落的数量和大小显著减少（观察到71.3±3.2个集落，而预测为231.2±38.5个集落），而去除Mo（BM-Mo）则未观察到此类变化；将自体T细胞与同时去除Mo和T细胞的BM（BM-Mo-T）共培养导致CFU-Mk衍生集落显著增加并恢复集落大小。向BM中添加γ-IFN（小于50-10,000 IU/ml）导致CFU-Mk呈剂量依赖性抑制（0-90%），集落数量减少和集落大小减小证明了这一点。向BM-T中添加γ-IFN（50-10,000 IU/ml）导致对CFU-Mk的抑制作用降低（0-60%）；将预先用γ-IFN（10,000 IU/ml；1小时，37℃，然后洗涤3次）孵育的T细胞（但不是Mo）共培养导致CFU-Mk受到抑制（添加1:4的T细胞：骨髓细胞时抑制80%）。结果表明，T细胞具有在体外调节人CFU-Mk生长的能力，并且在适当条件下，可能促进（正常T细胞）或抑制（γ-IFN激活的T细胞）人巨核细胞生成。
