巨噬细胞在登革病毒诱导的抑制信号向T淋巴细胞传递中的体内作用。
In vivo role of macrophages in transmission of dengue virus-induced suppressor signal to T lymphocytes.
作者信息
Shukla M I, Chaturvedi U C
出版信息
Br J Exp Pathol. 1982 Oct;63(5):522-30.
Dengue type 2 virus (DV)-induced suppressor T cells (Ts1) produce a soluble suppressor factor (SF) which stimulates a subpopulation of T lymphocytes (Ts2) to produce prostaglandin which suppresses DV-specific IgM antibody plaque forming cells (PFC) in vivo and in vitro. The present study was undertaken to investigate the intermediary role of macrophages in transmission of signal from Ts1 to Ts2. The SF is adsorbed on live or heat-killed mouse peritoneal macrophages and transmits DV-specific PFC in spleen after i.p. or i.v. inoculation in DV-primed mice. The suppression is antigen-specific. SF or SF-adsorbed heat-killed macrophages failed to transmit suppression in silica-treated macrophage-depleted mice when injected i.p., while SF-adsorbed live macrophages could transmit suppression. In macrophage-depleted mice suppression could be transmitted by SF-adsorbed heat-killed macrophages on i.v. inoculation. It was therefore concluded that live macrophage-killed cells are also essential for transmission of suppressor signal by SF from Ts1 to Ts2 in vivo.
2型登革病毒（DV）诱导的抑制性T细胞（Ts1）产生一种可溶性抑制因子（SF），该因子刺激T淋巴细胞亚群（Ts2）产生前列腺素，后者在体内和体外均可抑制DV特异性IgM抗体空斑形成细胞（PFC）。本研究旨在探讨巨噬细胞在信号从Ts1传递至Ts2过程中的中介作用。SF吸附于活的或热灭活的小鼠腹腔巨噬细胞上，并在经DV免疫的小鼠腹腔注射或静脉注射后，传递至脾脏中的DV特异性PFC。这种抑制是抗原特异性的。当腹腔注射时，SF或吸附有SF的热灭活巨噬细胞在经二氧化硅处理的巨噬细胞耗竭小鼠中无法传递抑制作用，而吸附有SF的活巨噬细胞可以传递抑制作用。在巨噬细胞耗竭的小鼠中，静脉注射吸附有SF的热灭活巨噬细胞可以传递抑制作用。因此得出结论，活巨噬细胞杀伤的细胞对于SF在体内将抑制信号从Ts1传递至Ts2也是必不可少的。
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