Okuda T, Tachibana T
Immunology. 1980 Sep;41(1):159-66.
Raji cells in our laboratory did not form rosettes with EAC43hu. When EAC43hu are treated with beta 1H, the treated EAC43hu forms heavy rosettes with Raji cells. Evidence is presented to show that these rosettes resulted from a new type of C3 receptor which is different from either CR1 (C3b receptor), CR2 (C3d receptor) or CR3 (C3bi receptor). Three lines of evidence clearly showed that C3 is implicated in the new rosette formation. C3 receptors isolated from human erythrocytes inhibited the new rosette formation, while they did not inhibit the rosette formation of Daudi cells via CR2, indicating that the new rosette-forming receptor is different from CR2. Anti-Raji cells antiserum inhibited the new rosette formation while it did not inhibit the reaction between human erythrocytes and EAC43 via CR1. This fact indicates that the new rosette-forming receptor is different from CR1 in accordance with the lack of rosette formation of Raji cells with EAC43. The evidence to differentiate the receptor from CR3 comes from no participation of C3b inactivator in the generation of rosette-forming activity of EAC43. Both the mode of action of anti-beta 1H and the effect of modification of bound C3b by N-bromosuccinimide suggest that EAC43 reacts with beta 1H, which in turn results in a conformational change of C3b. Raji cells might have receptors for the beta 1H altered C3b.
我们实验室的Raji细胞不与EAC43hu形成玫瑰花结。当用β1H处理EAC43hu时，处理后的EAC43hu与Raji细胞形成大量玫瑰花结。有证据表明，这些玫瑰花结是由一种新型的C3受体形成的，该受体不同于CR1（C3b受体）、CR2（C3d受体）或CR3（C3bi受体）。三条证据清楚地表明C3参与了新玫瑰花结的形成。从人红细胞中分离出的C3受体抑制了新玫瑰花结的形成，而它们并未通过CR2抑制Daudi细胞的玫瑰花结形成，这表明新的形成玫瑰花结的受体不同于CR2。抗Raji细胞抗血清抑制了新玫瑰花结的形成，而它并未通过CR1抑制人红细胞与EAC43之间的反应。这一事实表明，根据Raji细胞与EAC43缺乏玫瑰花结形成，新的形成玫瑰花结的受体不同于CR1。将该受体与CR3区分开来的证据来自于C3b灭活剂不参与EAC43形成玫瑰花结活性的产生。抗β1H的作用方式以及N-溴代琥珀酰亚胺对结合的C3b的修饰作用均表明EAC43与β1H反应，进而导致C3b的构象变化。Raji细胞可能具有针对β1H改变的C3b的受体。
