Combined studies of complement receptor and surface immunoglobulin-bearing cells and sheep erythrocyte rosette-forming cells in normal and leukemic human lymphocytes.

Combined studies of complement receptor and surface immunoglobulin-bearing cells and sheep erythrocyte rosette-forming cells in normal and leukemic human lymphocytes.
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正常和白血病人淋巴细胞中补体受体和表面免疫球蛋白携带细胞以及绵羊红细胞玫瑰花结形成细胞的联合研究。

DOI:
10.1172/jci107194
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发表时间:
1973
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
H. Grey
H. Grey
中科院分区:
--
文献类型:
--
作者:
G. D. Ross;E. Rabellino;M. Polley;H. Grey

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本文研究了正常人外周血、胸腺、脾脏、胸导管和慢性淋巴细胞白血病患者外周血淋巴细胞的补体受体位点(CRL)、表面免疫球蛋白(SIg)和与绵羊红细胞形成补体的能力(TRFC)。发现两种B细胞标志物(CRL和SIG)存在重叠,但不完全相同,而能够形成ROR的细胞存在于完全不相关的淋巴细胞群体中;因此,TRFC可能是T细胞的可靠标志物。在外周血中,24%的淋巴细胞具有SIg,但其中只有一半也是CRL。几乎所有的非SIg外周血淋巴细胞都是TRFC。在脾脏和胸导管中,仅观察到少数淋巴细胞具有SIg而不是CRL。另一方面,在所研究的三个脾中的两个中,10-20%的细胞是不具有SIg的CRL。在胸导管中,所有无SIG的非CRL。在胸导管中,所有非CRL、非SIg细胞均为TRFC。在慢性淋巴细胞白血病中有三个发现:(a)CRL的存在或不存在与是否存在SIg无关,因此在细胞为非SIg的个体中。CRL通常很丰富。(b)白血病细胞TRFC基本呈阴性。(c)与小鼠C3相比,白血病细胞与人C3的反应较差,EACmo检测到的CRL比EACu多20倍。后者的发现是在鲜明的对比,正常的CRL反应有点优先与EACu。这些数据表明,改变的表面IG受体和补体受体存在于慢性淋巴白血病细胞。由于从本研究中检测的所有白血病患者中获得的细胞在其细胞的高百分比中具有补体受体或表面免疫球蛋白,并且TRFC基本上为阴性,因此强烈提示白血病淋巴细胞是B细胞来源的。发现淋巴细胞仅具有两种B细胞标志物中的一种表明这些标志物并不均匀地存在于所有B细胞上,并且根据来源,一种或另一种可能是缺陷的。
Human lymphocytes from normal peripheral blood, thymus, spleen, thoracic duct, and peripheral lymphocytes from patients with chronic lymphatic leukemia were studied for complement receptor sites (CRL), surface immunoglobulin (SIg), and for the ability to form rosettes with sheep erythrocytes (TRFC). The two B cell markers (CRL and SIg) were found to be in overlapping, but not totally identical populations, whereas cells that were able to form rosettes were found in a totally unrelated population of lymphocytes; TRFC is therefore probably a reliable marker for T cells. In peripheral blood 24% of lymphocytes had SIg, but only half of these were also CRL. Almost all of the non-SIg peripheral blood lymphocytes were TRFC. In the spleen and thoracic duct only a few lymphocytes were observed that had SIg and were not CRL. On the other hand, in two of three spleens studied 10-20% of cells were CRL that did not have SIg. In the thoracic duct all non-CRL that did not have SIg. In the thoracic duct all non-CRL, non-SIg cells were TRFC. In chronic lymphatic leukemia three findings were made: (a) The presence or absence of CRL was independent of the presence or absence of SIg so that in individuals whose cells were non-SIg. CRL were usually plentiful. (b) Leukemic cells were essentially negative for TRFC. (c) Leukemic cells reacted poorly with human C3 compared to mouse C3, EACmo detecting up to 20-fold more CRL than EAChu. This latter finding was in sharp contrast to normal CRL that reacted somewhat preferentially with EAChu. These data suggest that altered surface Ig receptors and complement receptors are present in chronic lymphatic leukemic cells. Since the cells obtained from all leukemic patients tested in this study had either the complement receptor or surface immunoglobulin in a high percentage of their cells and were essentially negative for TRFC, it is strongly suggested that leukemic lymphocytes are of B cell origin. The finding of lymphocytes with only one of the two B cell markers suggests that these markers are not uniformly present on all B cells and that depending on the source, one or the other may be deficient.