Hamaguchi H, Takano N, Saito K, Enokihara H, Furusawa S, Shishido H
Department of Internal Medicine, Musashino Red Cross Hospital, Tokyo, Japan.
Br J Haematol. 1990 Sep;76(1):12-20. doi: 10.1111/j.1365-2141.1990.tb07830.x.
Autologous or allogeneic peripheral blood T cells can stimulate the human megakaryocyte progenitor cell (CFU-Meg)-derived colony formation in a dose-dependent fashion in agar cultures of nonadherent (NA), T cell-depleted (NT) bone marrow (BM) cells. Low concentrations of monocytes and T cells can collaborate in the stimulation of CFU-Meg colony formation or in the production of megakaryocyte colony stimulating factor (Meg-CSF) by T cells in the presence of mitogens or IL-2. Monocytes alone can produce only negligible Meg-CSF under any conditions. When monocyte conditioned medium (CM) was added to T cell-stimulated NA, NT BM cell cultures, CFU-Meg colony growth was appreciably increased compared with that stimulated by T cells alone. Dose-dependent increase in CFU-Meg colony growth was noted when varying concentrations of IL-1 were added to T cell-stimulated NA, NT cell cultures, although IL-1 itself could support no CFU-Meg colony growth in the absence of T cells. These data suggest that a synergistic interaction between T cells and monocytes during the production of Meg-CSF by T cells could be partly mediated by IL-1. IL-2 was found to stimulate Meg-CSF production by T cells in the presence or absence of mitogens. IL-2-stimulated Meg-CSF production by T cells was augmented by the addition of monocytes. Although IL-2 itself had no stimulatory effect on CFU-Meg colony growth, dramatic augmentation in the CFU-Meg colony number was noted when IL-2 was added to T cell-stimulated NA, NT cell cultures. High concentrations of monocytes and prostaglandin E (PGE) inhibited the CFU-Meg colony formation. These results suggest that IL-1 and IL-2 may play a stimulatory role on the normal human in vitro megakaryocytopoiesis, and may be involved in the development of reactive thrombocytosis and bone marrow megakaryocytic hyperplasia in various inflammatory diseases.
在非贴壁（NA）、T细胞去除（NT）的骨髓（BM）细胞的琼脂培养中，自体或异体外周血T细胞能以剂量依赖方式刺激人巨核细胞祖细胞（CFU-Meg）衍生的集落形成。低浓度的单核细胞和T细胞在有丝分裂原或白细胞介素-2存在的情况下，可协同刺激CFU-Meg集落形成或T细胞产生巨核细胞集落刺激因子（Meg-CSF）。在任何条件下，单核细胞单独只能产生可忽略不计的Meg-CSF。当将单核细胞条件培养基（CM）添加到T细胞刺激的NA、NT骨髓细胞培养物中时，与单独由T细胞刺激相比，CFU-Meg集落生长明显增加。当向T细胞刺激的NA、NT细胞培养物中添加不同浓度的白细胞介素-1时，观察到CFU-Meg集落生长呈剂量依赖性增加，尽管在没有T细胞的情况下白细胞介素-1本身不能支持CFU-Meg集落生长。这些数据表明，T细胞产生Meg-CSF过程中T细胞与单核细胞之间的协同相互作用可能部分由白细胞介素-1介导。发现白细胞介素-2在有或没有有丝分裂原的情况下都能刺激T细胞产生Meg-CSF。添加单核细胞可增强白细胞介素-2刺激T细胞产生Meg-CSF的作用。尽管白细胞介素-2本身对CFU-Meg集落生长没有刺激作用，但当将白细胞介素-2添加到T细胞刺激的NA、NT细胞培养物中时，CFU-Meg集落数量显著增加。高浓度的单核细胞和前列腺素E（PGE）抑制CFU-Meg集落形成。这些结果表明，白细胞介素-1和白细胞介素-2可能对正常人的体外巨核细胞生成起刺激作用，并可能参与各种炎症性疾病中反应性血小板增多症和骨髓巨核细胞增生的发生发展。
