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免疫介导的破坏作为持续性感染小鼠中LCMV诱导贫血机制的证据。

Evidence for immune-mediated destruction as mechanism for LCMV-induced anemia in persistently infected mice.

作者信息

Stellrecht-Broomhall K A

机构信息

Department of Biology, Rensselaer Polytechnic Institute, Troy, New York.

出版信息

Viral Immunol. 1991 Winter;4(4):269-80. doi: 10.1089/vim.1991.4.269.

DOI:10.1089/vim.1991.4.269
PMID:1668061
Abstract

A docile substrain of lymphocytic choriomeningitis virus (LCMV) causes a persistent infection in adult C3HeB mice and induces a severe anemia, which, unlike the viremia, eventually resolves. Measurements of red blood cell (RBC) survival rates demonstrated an increased rate of RBC clearance in these animals, indicating a hemolytic process for the anemia. Normal clearance rates of RBCs from infected mice transfused into control mice suggested that there was not an intrinsic defect in these cells. It also appeared that RBC destruction was immune-mediated, as cyclophosphamide treatments prevented the onset of anemia in infected mice, whereas adoptive transfer (AT) of immune splenocytes into immunocompromised mice reestablished the condition. The AT experiments also demonstrated that the onset of anemia correlated with the functional state of the immune cells. In addition, opsonization of RBCs was demonstrated by macrophage phagocytosis, and the appearance of opsonized RBCs corresponded with the course of the anemia. These findings support a hypothesis of RBC opsonization and subsequent phagocytosis by macrophages of the reticuloendothelial system as the mechanism for RBC destruction in LCMV-induced hemolytic anemia.

摘要

淋巴细胞性脉络丛脑膜炎病毒(LCMV)的一种温顺亚株可在成年C3HeB小鼠中引起持续性感染,并诱发严重贫血,与病毒血症不同的是,这种贫血最终会消退。红细胞(RBC)存活率的测量结果表明,这些动物的红细胞清除率有所增加,这表明贫血是一个溶血过程。将感染小鼠的红细胞输注到对照小鼠体内后,红细胞的清除率正常,这表明这些细胞没有内在缺陷。红细胞破坏似乎也是免疫介导的,因为环磷酰胺治疗可防止感染小鼠出现贫血,而将免疫脾细胞过继转移(AT)到免疫受损小鼠体内则会使贫血症状再次出现。AT实验还表明,贫血的发生与免疫细胞的功能状态相关。此外,巨噬细胞吞噬作用证明了红细胞的调理作用,调理红细胞的出现与贫血病程一致。这些发现支持了这样一种假说,即红细胞被调理后,随后被网状内皮系统的巨噬细胞吞噬,这是LCMV诱导的溶血性贫血中红细胞破坏的机制。

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