阿留申貂病细小病毒对K562细胞的感染是抗体依赖性的，并通过Fc（γ）RII受体介导。

Aleutian mink disease parvovirus infection of K562 cells is antibody-dependent and is mediated via an Fc(gamma)RII receptor.

作者信息

Dworak L J, Wolfinbarger J B, Bloom M E

机构信息

Laboratory of Persistent Viral Diseases, National Institutes of Health, Hamilton, Montana 59840, U.S.A.

出版信息

Arch Virol. 1997;142(2):363-73. doi: 10.1007/s007050050082.

DOI:10.1007/s007050050082

PMID:9125049

Abstract

Aleutian mink disease parvovirus (ADV) infects macrophages but infection is restricted. Using the human macrophage cell line U937, we reported infection to be antibody-dependent [22,23]. Recently, we learned that the U937 cells were contaminated with the human cell line, K562 [12]. To clarify which cell line actually supported ADV infection, we studied the antibody-dependent enhancement (ADE) of ADV infection in pure lines of U937 and K562. After infection with ADV complexed with mink anti-ADV antibody, up to 10% of the K562 cells, but none of the U937 cells showed evidence of infection. These results indicated that K562 cells, but not U937 cells, were susceptible to ADV. ADV-infected cultures of K562 were sorted by flow cytometry after staining with a murine monoclonal antibody (IV.3) directed against Fc(gamma)RII. Only cells that were IV.3 positive supported ADV gene expression. Also, preincubation of K562 cells with IV.3 blocked ADV infection by more than 90%. These results established that the ADE of ADV in K562 is Fc(gamma)RIIA-mediated.

摘要

阿留申貂病细小病毒（ADV）可感染巨噬细胞，但感染受到限制。我们曾利用人巨噬细胞系U937报道过该感染是抗体依赖性的[22,23]。最近，我们了解到U937细胞被人细胞系K562污染了[12]。为了明确哪种细胞系实际支持ADV感染，我们研究了ADV在U937和K562纯系中的抗体依赖性增强（ADE）作用。用与水貂抗ADV抗体复合的ADV感染后，高达10%的K562细胞呈现感染迹象，而U937细胞均未出现感染迹象。这些结果表明，K562细胞而非U937细胞对ADV敏感。用针对Fc（γ）RII的鼠单克隆抗体（IV.3）染色后，通过流式细胞术对ADV感染的K562培养物进行分选。只有IV.3阳性的细胞支持ADV基因表达。此外，用IV.3对K562细胞进行预孵育可使ADV感染减少90%以上。这些结果证实，K562中ADV的ADE是由Fc（γ）RIIA介导的。