Forbes I J, Zalewski P D, Valente L, Gee D
Clin Exp Immunol. 1982 Feb;47(2):396-404.
Using rosetting tests with untreated mouse erythrocytes (M) and pronase-treated M (pro M), four human B cell subsets can be identified. Three of these, possessing the phenotypes BM+ pro M+, BM- pro M+ or BM- pro M-, constitute 17%, 61% and 22% of normal blood B cells respectively. The fourth subset, BM+ pro M-, does not occur in normal tissues but was found in the pre-B-cell line of Raji cells, indicating that this phenotype may be a marker for early B cells. Some differences in the proportion of each subset were found in cord blood, lymph nodes and tonsils. Surface-immunoglobulin-positive (SIg+) and -negative (SIg-) non-T cells were present in each subset. M and pro-M rosetting tests were applied to cells from blood of 27 cases of chronic lymphocytic leukaemia (CLL) and to cells from involved nodes, spleen or marrow in five cases of non-Hodgkin's lymphoma (NHL). In 15 cases of CLL, there was considerable increase in the BM+ pro M+ subset (BM+ pro M+ type CLL); in seven cases, there was a predominance of BM- pro M+ cells and in another four cases, BM- pro M- cells predominated. All five cases of NHL were greatly enriched in BM- pro M- cells. There was no obvious correlation between rosetting and other surface markers but BM- pro M- clones in CLL or NHL always stained brightly with FITC-anti-Ig. This was not found in BM+ pro M+ or BM- pro M+ clones. Rosette formation of neuraminidase-treated B cells with M identifies the same subset as B-pro-M rosetting in normals and CLL. Evidence is presented that two types of receptors are involved in M and pro-M rosetting, designated R1 and R2, binding to corresponding M ligands L1 and L2. M rosetting is due to R1-L1 binding while R2-L2 binding mediates B-pro-M rosetting. Shifts between subsets within the same clone in some cases of CLL suggest that the subsets are distinct maturational stage of B-cell development rather than families of B cells of different lineage. The following B-cell maturation sequence is proposed: R1+ R2- lead to R1+ R2+ leads to R1- R2+ leads to R1- R2-.
使用未处理的小鼠红细胞（M）和链霉蛋白酶处理的M（pro M）进行玫瑰花结试验，可以识别出四个人类B细胞亚群。其中三个亚群，其表型分别为BM + pro M +、BM - pro M +或BM - pro M -，分别占正常血液B细胞的17%、61%和22%。第四个亚群BM + pro M -，在正常组织中不存在，但在Raji细胞的前B细胞系中发现，表明该表型可能是早期B细胞的标志物。在脐带血、淋巴结和扁桃体中发现了每个亚群比例的一些差异。每个亚群中都存在表面免疫球蛋白阳性（SIg +）和阴性（SIg -）的非T细胞。对27例慢性淋巴细胞白血病（CLL）患者血液中的细胞以及5例非霍奇金淋巴瘤（NHL）患者受累淋巴结、脾脏或骨髓中的细胞进行了M和pro - M玫瑰花结试验。在15例CLL患者中，BM + pro M +亚群显著增加（BM + pro M +型CLL）；在7例患者中，BM - pro M +细胞占优势，在另外4例患者中，BM - pro M -细胞占优势。所有5例NHL患者的BM - pro M -细胞均大量富集。玫瑰花结试验与其他表面标志物之间没有明显的相关性，但CLL或NHL中的BM - pro M -克隆总是用异硫氰酸荧光素抗Ig染色明亮。在BM + pro M +或BM - pro M +克隆中未发现这种情况。神经氨酸酶处理的B细胞与M的玫瑰花结形成在正常人和CLL中识别出与B - pro - M玫瑰花结相同的亚群。有证据表明，两种类型的受体参与M和pro - M玫瑰花结形成，分别命名为R1和R2，它们与相应的M配体L1和L2结合。M玫瑰花结形成是由于R1 - L1结合，而R2 - L2结合介导B - pro - M玫瑰花结形成。在某些CLL病例中，同一克隆内亚群之间的转变表明这些亚群是B细胞发育的不同成熟阶段，而不是不同谱系的B细胞家族。提出了以下B细胞成熟序列：R1 + R2 - 导致R1 + R2 + 导致R1 - R2 + 导致R1 - R2 -。
