Fc receptors for IgG, IgM and IgE on human leukaemic lymphocytes.
Fc receptors for IgG, IgM and IgE on human leukaemic lymphocytes.
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人白血病淋巴细胞上 IgG、IgM 和 IgE 的 Fc 受体。
DOI：
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发表时间：
1979
影响因子：
4.6
通讯作者：
Paul M Dainer
中科院分区：
文献类型：
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作者：
Hans L. Spiegelberg;Paul M Dainer
本文对17例慢性淋巴细胞性白血病(CLL)、1例淋巴肉瘤细胞白血病(LSL)、2例毛细胞白血病(HCL)、急性淋巴细胞性白血病(ALL)和Sezary综合征患者的淋巴细胞表面免疫球蛋白(Sig)和Fc受体进行了分析。用兔Ig G(EOAG)和Ig M(EOAM)抗EO抗体致敏的牛红细胞(EO)形成花环，检测Ig G和Ig M的Fc受体。用兔抗EO抗体Fab片段与IgE骨髓瘤蛋白(EOAE)的Fc片段组成的戊二醛偶联复合物包被EO，或用吸附了IgE的醛固定的EO包被EO来分析Fc受体。用Fab‘-抗EO与纯化的羊特异性抗体F(ab’)2片段包被的EO包被EO，检测Ig M、Ig D、Ig G、κ类Sigg和λ轻链型。
CLL、LSL和HCL患者淋巴细胞均有Fc受体表达(65±15%EOAG+，22·0±5·8%)。有10例患者在未过夜培养的情况下检测到大量具有IgM Fc受体的细胞(37±22%EOAM+，正常1.2±1.5%)。4例患者(2例慢性淋巴细胞性白血病，1例系统性红斑狼疮，1例肥厚性淋巴细胞性白血病)的淋巴细胞均有Fc-IgE受体，EOAE阳性率为22-88%，正常为1.8±0.7%。这4例患者中有3例的细胞也是EOAM+。大量的玫瑰花结细胞表明，单个淋巴细胞必须携带一类以上的Fc受体。ALL和Sezary综合征患者淋巴细胞Fc受体阳性细胞较少。
17例慢性淋巴细胞性白血病患者中，12例SIgM+和/或SIgD+，仅4例κ+或λ+，1例无SIG。1例肝细胞癌患者和1例肝细胞癌患者的细胞为SIgM+和SIgD+，而另1例肝细胞癌患者的细胞为SIGG，λ+。其他患者的sigg+细胞均未超过10%。ALL和Sezary综合征患者的Sig+和Fc受体阳性细胞数较少。
提示B细胞白血病患者的淋巴细胞可同时携带不同类别的Fc受体，不同类别的Fc受体频率呈递减趋势。
Fc receptors for IgG, IgM, IgE and the cell surface immunoglobulins (SIg) were analysed on lymphocytes from seventeen patients with chronic lymphatic leukaemia (CLL), one with lympho-sarcoma cell leukaemia (LSL), two each with hairy cell leukaemia (HCL), acute lymphatic leukaemia (ALL) and Sezary syndrome. Fc receptors for IgG and IgM were detected by rosette formation with ox erythrocytes (EO) sensitized with rabbit IgG (EOAG) and IgM (EOAM) anti-EO antibodies, respectively. Fc receptors for IgE were analysed either with EO coated with glutaraldehyde coupled complexes consisting of rabbit Fab' fragments of anti-EO antibodies and Fc fragments of an IgE myeloma protein (EOAE), or with aldehyde fixed EO to which IgE was adsorbed. SIg of classes IgM, IgD, IgG and κ and λ light chain type were detected with EO coated with complexes consisting of Fab'-anti-EO and purified F(ab')2 fragments of specific goat antibodies.
Lymphocytes of all patients with CLL, LSL and HCL had Fc receptors for IgG (65±15% EOAG+, normal 22·0±5·8%). Ten patients had significant numbers of cells with IgM Fc receptors (37±22% EOAM+, normal 1·2±1·5%) which were detected without overnight culturing of the lymphocytes. Lymphocytes of four patients (two CLL, one LSL, one HCL) had Fc receptors for IgE (22–88% EOAE+, normal 1·8±0·7%). The cells of three of these four patients were also EOAM+. The high numbers of rosetting cells indicated that individual lymphocytes must have carried more than one class of Fc receptors. The lymphocytes of the ALL and Sezary syndrome patients had few Fc receptor positive cells.
Of the seventeen patients with CLL, twelve were SIgM+ and/or SIgD+, only four κ+ or λ+ and one had no SIg. The cells of the LSL and one of the HCL patients were SIgM+ and SIgD+, whilst the cells of the other HCL patient were SIgG, λ+. None of the other patients had more than 10% SIgG+ cells. The ALL and Sezary syndrome patients had low numbers of SIg+ and Fc receptor positive cells.
These data indicate that lymphocytes of patients with B-cell leukaemias can carry different classes of Fc receptors simultaneously; the different classes are found in a decreasing frequency of IgG>IgM>IgE.