首页> 外文期刊>Infection and immunity >Inhibition of binding, entry, or intracellular proliferation of Ehrlichia risticii in P388D1 cells by anti-E. risticii serum, immunoglobulin G, or Fab fragment.
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Inhibition of binding, entry, or intracellular proliferation of Ehrlichia risticii in P388D1 cells by anti-E. risticii serum, immunoglobulin G, or Fab fragment.

机译:抗E抑制P388D1细胞中的埃希氏毛虫结合,进入或细胞内增殖。 Risticii血清,免疫球蛋白G或Fab片段。

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The effects of equine antiserum, immunoglobulin G (IgG) specific for Ehrlichia risticii, and its Fab fragment on E. risticii binding to, internalization into, and proliferation in P388D1 cells were studied by immunofluorescence flow cytometry. Anti-E. risticii equine serum or IgG inhibited E. risticii at a stage beyond binding and internalization. In contrast, monovalent anti-E. risticii equine Fab fragments inhibited E. risticii binding and internalization into P388D1 cells. In the presence of control equine serum, IgG, or its Fab fragment, E. risticii cells were bound, were internalized and subsequently grew within P388D1 cells, and eventually destroyed the host cells as effectively as was the case without equine serum, IgG, or Fab fragments. Anti-E. risticii IgG but not normal horse IgG inhibited L-[14C]glutamine metabolism in Percoll gradient-purified E. risticii. These findings suggest that the Fab fragment of intact anti-E. risticii IgG blocks the ligands on E. risticii responsible for non-IgG-mediated internalization and diverts them to bind via the Fc receptor. Following Fc-mediated entry of E. risticii, the antibody interfered with the metabolic activity of E. risticii cells, rendering them incapable of proliferation in P388D1 cells and resulting in the eventual destruction of the organisms.
机译:通过免疫荧光流式细胞术研究了马抗血清,对埃希氏毛虫的特异性免疫球蛋白G(IgG)及其Fab片段对埃希氏毛虫结合,内化和在P388D1细胞中增殖的影响。反E。 Risticii马血清或IgG在超出结合和内在化的阶段抑制了E. risticii。相反,单价抗E。栗色马的Fab片段抑制了栗色大肠杆菌的结合并内化到P388D1细胞中。在存在对照马血清,IgG或其Fab片段的情况下,结合大肠杆菌,将其内化并随后在P388D1细胞内生长,并最终像不使用马血清,IgG或E一样有效地破坏宿主细胞。 Fab片段。反E。 risticii IgG,但正常马IgG不抑制Percoll梯度纯化的E.risticii中的L- [14C]谷氨酰胺代谢。这些发现表明完整的抗E的Fab片段。 risticii IgG阻断了E.risticii上的配体,这些配体负责非IgG介导的内化作用,并转移它们通过Fc受体结合。 Fc介导的埃里希氏菌进入后,抗体干扰埃里希氏菌细胞的代谢活性,使其无法在P388D1细胞中增殖,并最终破坏了生物。

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