Theofilopoulos A N, Dixon F J, Bokisch V A
J Exp Med. 1974 Oct 1;140(4):877-94. doi: 10.1084/jem.140.4.877.
In the present work we studied the expression of membrane-bound Ig (MBIg) as well as receptors for IgG Fc and complement on nine human lymphoblastoid cell lines. When MBIg and receptors for IgG Fc were compared, four categories of cell lines could be distinguished: (a) cell lines having both MBIg and receptors for IgG Fc, (b) cell lines having MBIg but lacking receptors for IgG Fc, (c) cell lines lacking MBIg but having receptors for IgG Fc, and (d) cell lines lacking both MBIg and receptors for IgG Fc. Two types of receptors for complement could be detected on the cell lines studied, one for C3-C3b and one for C3d. When sensitized red cells carrying C3b or C3d were used for rosette tests, three categories of cell lines could be distinguished: (a) cell lines having receptors for C3b and C3d, (b) cell lines having receptors only for C3d and (c) cell lines lacking both receptors. However, when a more sensitive immunofluorescent method was used instead of the rosette technique, it was found that cell lines unable to form rosettes with EAC1423b(hu) were able to bind soluble C3 or C3b which indicated the presence of these receptors on the cell surface. Inhibition experiments showed that receptors for C3-C3b and receptors for C3d are distinct and that receptors for C3-C3b and C3d are different from receptors for IgG Fc. A cell line (Raji) without MBIg but with receptors for IgG Fc, C3-C3b, and C3d was selected for use in studying the binding mechanism of soluble immune complexes to cell surface membrane. Aggregated human gamma globulin was used in place of immune complexes. Immune complexes containing complement bind to Raji cells only via receptors for complement, namely receptors for C3-C3b and C3d. Binding of immune complexes containing complement to cells is much greater than that of complexes without complement. Immune complexes bound to cells via receptors for complement can be partially released from the cell surface by addition of normal human serum as well as isolated human C3 or C3b. We postulate that such release is due to competition of immune complex bound C3b and free C3 or C3b for the receptors on Raji cells.
在本研究中,我们研究了9种人淋巴母细胞系上膜结合免疫球蛋白(MBIg)以及IgG Fc和补体受体的表达。比较MBIg和IgG Fc受体时,可区分出四类细胞系:(a)既有MBIg又有IgG Fc受体的细胞系;(b)有MBIg但缺乏IgG Fc受体的细胞系;(c)缺乏MBIg但有IgG Fc受体的细胞系;(d)既缺乏MBIg又缺乏IgG Fc受体的细胞系。在所研究的细胞系上可检测到两种补体受体,一种是C3 - C3b受体,另一种是C3d受体。当用携带C3b或C3d的致敏红细胞进行玫瑰花结试验时,可区分出三类细胞系:(a)有C3b和C3d受体的细胞系;(b)仅有C3d受体的细胞系;(c)两种受体均缺乏的细胞系。然而,当使用更灵敏的免疫荧光法代替玫瑰花结技术时,发现不能与EAC1423b(hu)形成玫瑰花结的细胞系能够结合可溶性C3或C3b,这表明这些受体存在于细胞表面。抑制实验表明,C3 - C3b受体和C3d受体是不同的,且C3 - C3b和C3d受体与IgG Fc受体也不同。选择了一个无MBIg但有IgG Fc、C3 - C3b和C3d受体的细胞系(Raji)用于研究可溶性免疫复合物与细胞表面膜的结合机制。用聚合人γ球蛋白代替免疫复合物。含补体的免疫复合物仅通过补体受体,即C3 - C3b和C3d受体与Raji细胞结合。含补体的免疫复合物与细胞的结合比不含补体的复合物强得多。通过补体受体与细胞结合的免疫复合物可通过加入正常人血清以及分离的人C3或C3b从细胞表面部分释放。我们推测这种释放是由于免疫复合物结合的C3b与游离的C3或C3b竞争Raji细胞上的受体所致。