Characterization of the C3 receptor induced by herpes simplex virus type 1 infection of human epidermal, endothelial, and A431 cells.
Characterization of the C3 receptor induced by herpes simplex virus type 1 infection of human epidermal, endothelial, and A431 cells.
复制标题
1 型单纯疱疹病毒感染人表皮、内皮和 A431 细胞诱导的 C3 受体的表征。
作者：
Y. Kubota;T. Gaither;J. Cason;J. O’Shea;T. Lawley
单纯疱疹病毒1型（HSV-1）感染诱导人Fc IgG和C3受体的病毒类似物在人细胞表面上出现。病毒诱导的C3受体已被广泛定义为C3 b受体，但其配体结合特征尚未严格定义。在这项研究中，感染HSV-1的人表皮细胞、A431细胞和人脐静脉内皮细胞表现出与IgG（E-IgG）或补体成分C3 b（EAC 3b）或iC 3b（EAC 3bi）包被的绵羊红细胞（E）的玫瑰花结，但不与E-IgM、C4（EAC 14）、C3 d（EAC 3d）或单独的E包被。用神经氨酸酶预处理HSV-1感染的细胞显著增强了玫瑰花结。与人C3受体不同，发现HSV-1诱导的C3受体具有胰蛋白酶抗性。为了确定HSV-1是否诱导CR 1样受体或CR 3样受体，用已知可抑制天然CR 3功能的EDTA预处理感染的细胞。EDTA未能阻止EAC 3bi的玫瑰花结。此外，使用针对CR 1和CR 3的单克隆抗体进行的阻断研究显示，抗CR 1抗体5C 11以剂量依赖性方式持续阻断EAC 3b和EAC 3与HSV-1感染细胞的双花环形成，但针对CR 3的单克隆抗体没有。这项研究表明，HSV-1诱导的C3受体是CR 1的类似物。
Herpes simplex virus type 1 (HSV-1) infection induces the appearance of viral analogues of human Fc IgG and C3 receptors on the surface of human cells. The virally induced C3 receptor(s) has been broadly defined as a C3b receptor, but its ligand binding characteristics have not been rigorously defined. In this study, human epidermal cells, A431 cells, and human umbilical vein endothelial cells infected with HSV-1 demonstrated rosetting with sheep erythrocytes (E) coated with IgG (E-IgG) or the complement components C3b (EAC3b) or iC3b (EAC3bi), but not with E-IgM, C4 (EAC14), C3d (EAC3d), or E alone. Rosetting was markedly enhanced by pretreatment of HSV-1-infected cells with neuraminidase. Unlike human C3 receptors, the HSV-1-induced C3 receptor was found to be trypsin resistant. To determine whether HSV-1 induced CR1-like receptors or CR3-like receptors, infected cells were pretreated with EDTA, which is known to inhibit native CR3 function. EDTA failed to prevent rosetting with EAC3bi. Furthermore, blocking studies using monoclonal antibodies against CR1 and CR3 revealed that the anti-CR1 antibody 5C11 consistently blocked EAC3b and EAC3bi rosetting with HSV-1-infected cells in a dose dependent manner, but monoclonal antibodies against CR3 did not. This study indicates that the HSV-1-induced C3 receptor is an analogue of CR1.