Jungi T W, McGregor D D
Infect Immun. 1979 Mar;23(3):633-43. doi: 10.1128/iai.23.3.633-643.1979.
The hypothesis was tested that delayed-type hypersensitivity (DTH) to the complement-activating bacterium Listeria monocytogenes is initiated by complement-derived mediators that attract sensitized lymphocytes to reaction sites. To this end DTH and acquired resistance to L. monocytogenes were measured in rats injected with cobra venom factor, a potent inactivator of C3. Treatment with cobra venom factor reduced the hemolytic power of serum to less than 0.5% of the control value. Such decomplemented animals expressed both DTH and antimicrobial resistance, although expression of DTH was reduced (ca. 50%) when compared with complement-sufficient controls. The observed depression of DTH in cobra venom factor-treated rats was associated with a reduction in the number of recently activated lymphocytes (lymphoblasts) and macrophages that accumulated in DTH reaction sites. The above findings are explained, in part, by inhibition of inflammation during the early postinduction period. Supporting evidence came from measurements of labeled lymphoblast sequestration in saline injection sites and the slower accumulation of macrophages in nitrocellulose filters that were implanted subcutaneously in complement-depleted rats. The ability of cobra venom factor-treated rats to express DTH and protect themselves against a Listeria challenge seems to exclude C3-dependent factors as essential mediators in the attraction of antigen-reactive lymphocytes to reaction sites.
有人提出一种假说，即对补体激活细菌单核细胞增生李斯特菌的迟发型超敏反应（DTH）是由补体衍生的介质引发的，这些介质将致敏淋巴细胞吸引到反应部位。为此，在注射了眼镜蛇毒因子（一种有效的C3灭活剂）的大鼠中测量了DTH和对单核细胞增生李斯特菌的获得性抵抗力。用眼镜蛇毒因子处理后，血清的溶血能力降低到对照值的0.5%以下。这些补体缺失的动物同时表现出DTH和抗菌抵抗力，尽管与补体充足的对照组相比，DTH的表达有所降低（约50%）。在眼镜蛇毒因子处理的大鼠中观察到的DTH降低与在DTH反应部位积累的近期活化淋巴细胞（成淋巴细胞）和巨噬细胞数量减少有关。上述发现部分可以通过诱导后早期炎症的抑制来解释。支持性证据来自于对盐水注射部位标记的成淋巴细胞滞留的测量，以及在补体缺失的大鼠皮下植入的硝酸纤维素滤膜中巨噬细胞积累较慢的情况。眼镜蛇毒因子处理的大鼠表达DTH并保护自己免受李斯特菌攻击的能力似乎排除了C3依赖性因子作为将抗原反应性淋巴细胞吸引到反应部位的必需介质。
