Isaak D D, Fleischmann R, Cerny J
Department of Molecular Biology, University of Wyoming, Laramie 82071.
Cell Immunol. 1989 May;120(2):375-86. doi: 10.1016/0008-8749(89)90205-0.
The ability of splenic T-cells to regulate Friend murine leukemia virus replication in lipopolysaccharide-activated target B-cells infected in vitro was investigated. Removal of the T-cell fraction from spleen cells resulted in an 8- to 10-fold enhancement in the number of productively infected cells in the remaining B-cell-enriched fraction, as compared with unseparated spleen cells, and the addition of increasing numbers of purified T-cells to isolated B-cells prior to infection resulted in a directly proportional reduction in the number of B-cells releasing infectious progeny virus. Separation of splenic T-cells into Lyt 2- and Lyt 2+ T-cells before addition to infected B-cell cultures resulted in inhibition of infection only with the Lyt 2- T-cells; Lyt 2+ T-cells did not inhibit infection, even at high 1:1 ratios. Similarly, separation of splenic T-cells into L3T4+ and L3T4- T-cells before addition resulted in inhibition by L3T4+ but not L3T4- T-cells. Also, cytotoxic treatment of splenic T-cells with monoclonal anti-L3T4 antibody and complement before addition to B-cell cultures destroyed the regulatory effects. Finally, depletion of macrophages from both T-cells and B-cells before infection and coculture had no effect on the ability of T-cells to regulate B-cell infection. Collectively these results demonstrate that L3T4+ T-cells can inhibit Friend murine leukemia virus replication in target B-cells. Culture of isolated splenic T-cells with Friend murine leukemia virus in vitro resulted in the induction of alpha/beta but not interferon-gamma synthesis and in some experiments interferon-containing supernatants from T-cell-virus cultures were able to mediate suppression of B-cell infection with Friend helper virus; the addition of antibody specific for interferon-alpha/beta to cultures inhibited the ability of T-cells to regulate B-cell infection.
研究了脾T细胞在体外对脂多糖激活的、被感染的靶B细胞中Friend小鼠白血病病毒复制的调节能力。从脾细胞中去除T细胞部分,与未分离的脾细胞相比,剩余富含B细胞的部分中产生感染性病毒的细胞数量增加了8到10倍,并且在感染前向分离的B细胞中添加数量不断增加的纯化T细胞,导致释放感染性子代病毒的B细胞数量成比例减少。在将脾T细胞添加到受感染的B细胞培养物之前,将其分离为Lyt 2 -和Lyt 2 + T细胞,结果仅Lyt 2 - T细胞能抑制感染;即使Lyt 2 + T细胞与B细胞的比例高达1:1,也不会抑制感染。同样,在添加之前将脾T细胞分离为L3T4 +和L3T4 - T细胞,结果L3T4 + T细胞能抑制感染,而L3T4 - T细胞则不能。此外,在将脾T细胞添加到B细胞培养物之前,用单克隆抗L3T4抗体和补体对其进行细胞毒性处理,会破坏其调节作用。最后,在感染和共培养之前从T细胞和B细胞中去除巨噬细胞,对T细胞调节B细胞感染的能力没有影响。这些结果共同表明,L3T4 + T细胞可以抑制靶B细胞中Friend小鼠白血病病毒的复制。体外将分离的脾T细胞与Friend小鼠白血病病毒一起培养,可诱导α/β干扰素的合成,但不会诱导γ干扰素的合成,并且在一些实验中,T细胞 - 病毒培养物中含干扰素的上清液能够介导对Friend辅助病毒感染B细胞的抑制作用;向培养物中添加针对α/β干扰素的特异性抗体,会抑制T细胞调节B细胞感染的能力。