INJECTION OF MICE WITH ANTIBODY TO INTERFERON RENDERS PERITONEAL-MACROPHAGES PERMISSIVE FOR VESICULAR STOMATITIS-VIRUS AND ENCEPHALOMYOCARDITIS VIRUS

INJECTION OF MICE WITH ANTIBODY TO INTERFERON RENDERS PERITONEAL-MACROPHAGES PERMISSIVE FOR VESICULAR STOMATITIS-VIRUS AND ENCEPHALOMYOCARDITIS VIRUS
复制标题

DOI:
10.1073/pnas.81.2.602
复制
发表时间:
1984-01-01
期刊:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子:
--
通讯作者:
GRESSER, I
GRESSER, I
中科院分区:
其他
文献类型:
--
作者:
BELARDELLI, F;VIGNAUX, F;GRESSER, I

文献摘要

被引文献

相似文献

水泡性口炎病毒(VSV)和脑心肌炎病毒(EMCV)在4-6周龄雄性或雌性DBA/2、BALB/c、C3 H、C57 BL/6或Swiss小鼠腹腔巨噬细胞中仅少量繁殖。当这些小鼠腹膜内注射有效的绵羊(或山羊)抗小鼠干扰素α 1时,β的在收获腹腔巨噬细胞前4天,用免疫球蛋白接种病毒,病毒倍增至高滴度,并且大多数细胞被感染,如通过总病毒产量(VSV和EMCV)、VSV抗原阳性细胞的百分比(免疫荧光)和VSV感染中心的测定所确定的。当小鼠接种其他绵羊超免疫球蛋白或正常血清球蛋白时,未观察到这种效应。抗干扰素球蛋白似乎在体内起作用,因为在细胞附着期间或病毒吸收后18小时内,将该球蛋白与腹腔巨噬细胞孵育,不会使这些细胞允许VSV。小鼠腹腔注射抗干扰素球蛋白不影响标记VSV与腹腔巨噬细胞的结合和摄取。虽然这种现象的潜在机制尚不清楚,但结果表明可能存在低水平的内源性干扰素,其通过维持某些细胞处于抗病毒状态而有助于宿主防御。
Vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV) multiply in only a small percentage of peritoneal macrophages freshly explanted from 4-6 wk old male or female DBA/2, BALB/c, C3H, C57BL/6 or Swiss mice. When these mice were injected i.p. with potent sheep (or goat) anti-mouse interferon .alpha./.beta. globulin 4 days prior to harvesting peritoneal macrophages, the viruses multipled to high titers and most of the cells were infected, as determined by total virus yield (VSV and EMCV), percentage of VSV antigen-positive cells (immunofluorescence) and determination of VSV infectious centers. This effect was not observed when mice were inoculated with other sheep hyperimmune or normal serum globulins. Anti-interferon globulin appeared to act in vivo because incubation of this globulin with peritoneal macrophages during the period of cell attachment, or during the 18 h after virus absorption, did not render these cells permissive for VSV. Injection of mice with anti-interferon globulin did not affect the binding and uptake of labeled VSV by peritoneal macrophages. Although the underlying mechanism of this phenomenon is unknown, the results suggest that there may be low levels of endogenous interferon that contribute to host defense by maintaining some cells in an antiviral state.