Perry L L, Lodmell D L
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.
J Virol. 1991 Jul;65(7):3429-34. doi: 10.1128/JVI.65.7.3429-3434.1991.
Mice of the SJL/J and BALB/cByJ inbred strains are naturally resistant to street rabies virus (SRV) injected via the intraperitoneal route. To determine the cellular mechanism of resistance, monoclonal antibodies specific for CD4+ or CD8+ subsets of T cells were used to deplete the respective cell population in SRV-infected animals. Elimination of CD4+ T-helper cells abrogated the production of immunoglobulin G (IgG) neutralizing antibodies in response to rabies virus infection and reversed the resistant status of SJL/J and BALB/cByJ mice. In contrast, in vivo depletion of CD8+ cytotoxic T cells had no measurable effect on host resistance to SRV. These results indicate that serum neutralizing antibodies of the IgG class are a primary immunological mechanism of defense against rabies virus infection in this murine model of disease. CD8+ cytotoxic T lymphocytes, which have been shown to transfer protection in other rabies virus systems, appear to have no role in protecting mice against intraperitoneally injected SRV.
SJL/J和BALB/cByJ近交系小鼠对经腹腔注射的街狂犬病毒（SRV）天然具有抗性。为了确定抗性的细胞机制，使用针对T细胞CD4+或CD8+亚群的单克隆抗体来清除SRV感染动物中的相应细胞群体。消除CD4+辅助性T细胞消除了狂犬病病毒感染后免疫球蛋白G（IgG）中和抗体的产生，并逆转了SJL/J和BALB/cByJ小鼠的抗性状态。相比之下，体内清除CD8+细胞毒性T细胞对宿主抵抗SRV没有可测量的影响。这些结果表明，IgG类血清中和抗体是该小鼠疾病模型中抵御狂犬病病毒感染的主要免疫防御机制。在其他狂犬病病毒系统中已显示能传递保护作用的CD8+细胞毒性T淋巴细胞，似乎在保护小鼠抵抗腹腔注射的SRV方面没有作用。
