Goldman M B, O'Bryan T A, Buckthal D J, Tetor L M, Goldman J N
Department of Medicine, Pennsylvania State University, Hershey 17033.
J Virol. 1995 Feb;69(2):734-40. doi: 10.1128/JVI.69.2.734-740.1995.
Immune regulation of measles virus (MV) expression was studied in a persistently infected mouse macrophage cell line. Synthesis of both membrane-associated and internal MV antigens was suppressed when infected macrophages were treated with polyclonal rabbit anti-MV antibody that was specific for MV proteins. Persistently infected macrophages were treated for 3, 5, or 7 days with increasing doses of anti-MV antibody. All MV proteins were down-regulated 2 days after treatment was terminated. One week after treatment was terminated, down-regulation was still evident but to a lesser degree. MV protein synthesis was suppressed whether or not complement components were inactivated by heating all serum supplements and antibodies. However, when complement was active, cell lysis accounted for some of the reduced MV protein synthesis. When lytic destruction of infected cells by antibody and complement was prevented by inactivation of complement, antibody alone reduced the cellular synthesis of viral proteins by noncytolytic mechanisms. The absence of cell death in the absence of complement was confirmed by the lack of 51Cr release from labeled cells, the lack of reduction in cell number, and the lack of a decrease in total protein synthesis when radiolabeled infected cells were treated with antibody. It is noteworthy that low doses of antibody were optimal for suppression in the longer-term experiments and did not cause lysis, even in the presence of active complement. Since infected macrophages disseminate virus in measles infection, noncytolytic regulation of these cells by antibody may supplement viral clearance by cytolytic T cells and other immune mechanisms.
在一个持续感染的小鼠巨噬细胞系中研究了麻疹病毒(MV)表达的免疫调节。当用对MV蛋白具有特异性的多克隆兔抗MV抗体处理感染的巨噬细胞时,膜相关和内部MV抗原的合成均受到抑制。用递增剂量的抗MV抗体对持续感染的巨噬细胞处理3、5或7天。处理终止后2天,所有MV蛋白均下调。处理终止1周后,下调仍然明显,但程度较小。无论所有血清补充剂和抗体是否通过加热使补体成分失活,MV蛋白合成均受到抑制。然而,当补体有活性时,细胞裂解是MV蛋白合成减少的部分原因。当通过补体失活防止抗体和补体对感染细胞的裂解破坏时,单独抗体通过非细胞溶解机制降低病毒蛋白的细胞合成。当用抗体处理放射性标记的感染细胞时,标记细胞缺乏51Cr释放、细胞数量没有减少以及总蛋白合成没有下降,证实了在没有补体的情况下没有细胞死亡。值得注意的是,在长期实验中,低剂量抗体最适合抑制,并且即使在有活性补体存在的情况下也不会引起裂解。由于感染的巨噬细胞在麻疹感染中传播病毒,抗体对这些细胞的非细胞溶解调节可能补充细胞溶解T细胞和其他免疫机制的病毒清除作用。