Harty J T, Schreiber R D, Bevan M J
Howard Hughes Medical Institute, Seattle, WA.
Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11612-6. doi: 10.1073/pnas.89.23.11612.
Specific T-cell immunity to Listeria monocytogenes is thought to occur through the action of lymphokines which activate phagocytes to ingest and kill microorganisms. Interferon gamma (IFN-gamma) has been shown to be an effective mediator of this type of macrophage activation in vivo and in vitro. The monoclonal antibody H22.1 efficiently neutralizes endogenous IFN-gamma, exacerbates disease in a mouse model of L. monocytogenes infection, and inhibits the in vivo protective activity of a Listeria antigen-specific CD4 T-cell line. In contrast, in vivo protection by Listeria-immune CD8 T cells is not inhibited by the neutralizing anti-IFN-gamma monoclonal antibody. These results suggest that CD8 T cells can protect against an intracellular pathogen in an IFN-gamma-independent manner.
针对单核细胞增生李斯特菌的特异性T细胞免疫被认为是通过淋巴因子的作用而发生的，这些淋巴因子激活吞噬细胞以摄取和杀死微生物。γ干扰素（IFN-γ）已被证明是体内和体外这种巨噬细胞激活类型的有效介质。单克隆抗体H22.1能有效中和内源性IFN-γ，在单核细胞增生李斯特菌感染的小鼠模型中加重疾病，并抑制李斯特菌抗原特异性CD4 T细胞系的体内保护活性。相比之下，李斯特菌免疫的CD8 T细胞的体内保护作用不受中和性抗IFN-γ单克隆抗体的抑制。这些结果表明，CD8 T细胞可以以不依赖IFN-γ的方式抵御细胞内病原体。
