Lu L, Pelus L M, Broxmeyer H E, Moore M A, Wachter M, Walker D, Platzer E
Blood. 1986 Jul;68(1):126-33.
The relationship between major histocompatibility complex class II antigens (MHC class II, eg, HLA-DR, Ia), T lymphocytes, and the enhancement of erythroid colony formation from BFU-E by prostaglandin E was analyzed using normal bone marrow cells. In primary methylcellulose culture, the addition of prostaglandin E1 (PGE1) to unseparated buffy coat, low-density, or nonadherent low-density (NAL) marrow cells resulted in an enhancement of the total number of erythroid (BFU-E) colonies observed. Treatment of bone marrow cells with a monoclonal antihuman MHC class II antibody plus complement (C') resulted in a reduction of the total number of colonies by approximately 50% and abrogation of the enhancing effect of PGE1. Analysis of accessory cell requirements by depletion of both adherent cells and sheep erythrocyte rosetting lymphocytes (E+ cells) and reconstitution using C' or anti-MHC class II antibody plus C'-treated T cell-depleted NAL (NALT-) marrow cells and E+ cell populations treated with C' or anti-MHC class II antibody plus C' demonstrated a requirement for MHC class II antigen-T cells, but not adherent cells, and a requirement for MHC class II antigen + BFU-E in order to observe the enhancing effect of PGE1 on erythroid colony formation. Positive selection of BFU-E in NALT- bone marrow expressing differing density distributions of MHC class II antigens was accomplished with monoclonal anti-MHC class II antibodies and sorting with a fluorescence-activated cell sorter (FACS). Addition of E+ cells to the different populations of MHC class II antigen+ NALT- cells demonstrated that the PGE-enhancing effects on erythroid colony formation were directly related to increasing density distributions of MHC class II antigens on BFU-E. Colony formation by BFU-E expressing a low density distribution of MHC class II antigens or having no detectable MHC class II antigens, as determined by FACS analysis, was not enhanced by PGE1 in the presence of MHC class II antigen-positive or -negative T cells.
利用正常骨髓细胞分析了主要组织相容性复合体II类抗原（MHC II类，如HLA-DR、Ia）、T淋巴细胞以及前列腺素E对BFU-E红系集落形成的增强作用之间的关系。在原代甲基纤维素培养中，向未分离的血沉棕黄层、低密度或非贴壁低密度（NAL）骨髓细胞中添加前列腺素E1（PGE1），可使观察到的红系（BFU-E）集落总数增加。用单克隆抗人MHC II类抗体加补体（C'）处理骨髓细胞，可使集落总数减少约50%，并消除PGE1的增强作用。通过去除贴壁细胞和绵羊红细胞花环形成淋巴细胞（E+细胞）并使用C'或抗MHC II类抗体加C'处理的T细胞耗尽的NAL（NALT-）骨髓细胞和用C'或抗MHC II类抗体加C'处理的E+细胞群体进行重建来分析辅助细胞需求，结果表明需要MHC II类抗原-T细胞，但不需要贴壁细胞，并且需要MHC II类抗原+BFU-E才能观察到PGE1对红系集落形成有增强作用。用单克隆抗MHC II类抗体并通过荧光激活细胞分选仪（FACS）分选，对表达不同密度分布MHC II类抗原的NALT-骨髓中的BFU-E进行阳性选择。将E+细胞添加到不同的MHC II类抗原+NALT-细胞群体中表明，PGE对红系集落形成的增强作用与BFU-E上MHC II类抗原密度分布增加直接相关。通过FACS分析确定，表达低密度分布MHC II类抗原或无可检测MHC II类抗原的BFU-E的集落形成，在存在MHC II类抗原阳性或阴性T细胞的情况下，PGE1不会增强其集落形成。
