Klagge I M, ter Meulen V, Schneider-Schaulies S
Institute for Virology and Immunobiology, University of Würzburg, Germany.
Eur J Immunol. 2000 Oct;30(10):2741-50. doi: 10.1002/1521-4141(200010)30:10<2741::AID-IMMU2741>3.0.CO;2-N.
Measles virus (MV) infection promotes maturation of dendritic cells (DC), but also interferes with DC functions, and MV renders the DC inhibitory for T cell proliferation. We now describe that MV infection triggers the release of type I IFN from monocyte-derived DC (Mo-DC) which contributes to DC maturation. There is no evidence that soluble mediators are released interfering with the stimulatory activity of uninfected DC. Since inhibition of allogeneic T cell proliferation was unaffected by a fusion inhibitory peptide (Z-fFG), MV infection of T cells did not contribute to inhibition. Allogeneic T cell proliferation depended on the percentage of DC expressing MV F/H glycoproteins within the DC population and their surface expression levels, was induced upon addition of UV-inactivated MV to a mixed lymphocyte reaction stimulated by lipopolysaccharide-matured DC, and was not induced by DC infected with a recombinant MV encoding the ectodomain of vesicular stomatitis virus G protein (MG/FV) instead of the MV glycoproteins. Similarly, DC infected with MV, but not with MG/FV inhibited mitogen-induced proliferation of T cells. Thus, a dominant inhibitory signal is delivered to T cells by the MV glycoproteins on the surface of DC overcoming positive signals by co-stimulatory molecules promoted by maturation factors released from infected DC.
麻疹病毒（MV）感染可促进树突状细胞（DC）成熟，但也会干扰DC功能，并且MV会使DC对T细胞增殖产生抑制作用。我们现在描述MV感染会触发单核细胞衍生的DC（Mo-DC）释放I型干扰素，这有助于DC成熟。没有证据表明会释放可溶性介质干扰未感染DC的刺激活性。由于融合抑制肽（Z-fFG）对同种异体T细胞增殖的抑制没有影响，因此T细胞的MV感染对抑制作用没有贡献。同种异体T细胞增殖取决于DC群体中表达MV F/H糖蛋白的DC百分比及其表面表达水平，在向由脂多糖成熟的DC刺激的混合淋巴细胞反应中添加紫外线灭活的MV后可诱导增殖，而用编码水泡性口炎病毒G蛋白（MG/FV）胞外域而非MV糖蛋白的重组MV感染的DC则不会诱导增殖。同样，感染MV而非MG/FV的DC会抑制丝裂原诱导的T细胞增殖。因此，DC表面的MV糖蛋白会向T细胞传递一个占主导地位的抑制信号，从而克服由感染DC释放的成熟因子促进的共刺激分子产生的阳性信号。
