Giese N A, Giese T, Morse H C
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
J Virol. 1994 Sep;68(9):5819-24. doi: 10.1128/JVI.68.9.5819-5824.1994.
Murine AIDS (MAIDS) is a complex syndrome of lymphoproliferation and immunodeficiency induced by a replication-defective murine leukemia virus (BM5def) that encodes Pr60gag as its only product. It has been suggested that the gag polyprotein is responsible for vigorous antigenic stimulation of CD4+ T cells and generalized secondary activation of the immune system. This model was tested first by infecting mice (C2K/O) that lack class II major histocompatibility complex molecules required for presentation of antigens to CD4+ T cells. C2K/O mice expressed BM5def at high levels but did not develop MAIDS either when unmanipulated or following transfer of CD4+ T cells. Second, B6 mice reconstituted with C2K/O bone marrow cells had normal frequencies of B cells (class II negative) and CD4+ cells and expressed high levels of BM5def transcripts but did not develop MAIDS; however, MAIDS developed in class II-competent nu/nu mice reconstituted with CD4+ T cells and in C2K/O mice reconstituted with B6 bone marrow to give class II-positive B cells and with purified CD4+ T cells. These results indicate that induction of MAIDS by BM5def is antigen driven and is dependent on expression of major histocompatibility complex class II molecules on antigen-presenting cells and the presence of CD4+ T cells.
鼠艾滋病（MAIDS）是一种由复制缺陷型鼠白血病病毒（BM5def）诱导产生的淋巴增殖和免疫缺陷的复杂综合征，该病毒仅编码Pr60gag作为其唯一产物。有人提出，gag多聚蛋白负责对CD4 + T细胞进行强烈的抗原刺激以及免疫系统的全身性继发性激活。首先通过感染缺乏向CD4 + T细胞呈递抗原所需的II类主要组织相容性复合体分子的小鼠（C2K/O）来验证该模型。C2K/O小鼠高水平表达BM5def，但在未处理或转移CD4 + T细胞后均未发生MAIDS。其次，用C2K/O骨髓细胞重建的B6小鼠具有正常频率的B细胞（II类阴性）和CD4 +细胞，并高水平表达BM5def转录本，但未发生MAIDS；然而，用CD4 + T细胞重建的具有II类功能的nu/nu小鼠以及用B6骨髓重建以产生II类阳性B细胞并与纯化的CD4 + T细胞一起重建的C2K/O小鼠发生了MAIDS。这些结果表明，BM5def诱导MAIDS是抗原驱动的，并且依赖于抗原呈递细胞上主要组织相容性复合体II类分子的表达以及CD4 + T细胞的存在。
