Department of International Health, Immunology and Microbiology, University of Copenhagen, Copenhagen DK-2200, Denmark.
J Immunol. 2011 Apr 1;186(7):3997-4007. doi: 10.4049/jimmunol.1001251. Epub 2011 Feb 28.
The impact of prophylactic vaccination against acute and chronic infection in a Th-deficient host has not been adequately addressed because of difficulties in generating protective immunity in the absence of CD4(+) T cell help. In this study, we demonstrated that a broad CD8(+) T cell immune response could be elicited in MHC class II-deficient mice by vaccination with adenovirus encoding lymphocytic choriomeningitis virus (LCMV) glycoprotein tethered to MHC class II-associated invariant chain. Moreover, the response induced conferred significant cytolytic CD8(+) T cell-mediated protection against challenge with a high dose of the invasive clone 13 strain of LCMV. In contrast, vaccination with adenovirus encoding unlinked LCMV glycoprotein induced weak virus control in the absence of CD4(+) T cells, and mice may die of increased immunopathology associated with incomplete protection. Acute mortality was not observed in any vaccinated mice following infection with the less-invasive Traub strain. However, LCMV Traub infection caused accelerated late mortality in unvaccinated MHC class II-deficient mice; in this case, we observed a strong trend toward delayed mortality in vaccinated mice, irrespective of the nature of the vaccine. These results indicated that optimized vaccination may lead to efficient protection against acute viral infection, even in Th-deficient individuals, but that the duration of such immunity is limited. Nevertheless, for select immunodeficiencies in which CD4(+) T cell deficiency is incomplete or transient, these results are very encouraging.
由于在缺乏 CD4(+) T 细胞辅助的情况下难以产生保护性免疫,预防性接种疫苗以预防急性和慢性感染对 Th 缺陷宿主的影响尚未得到充分解决。在这项研究中,我们证明,通过用编码与 MHC Ⅱ类相关的不变链连接的淋巴细胞性脉络丛脑膜炎病毒 (LCMV) 糖蛋白的腺病毒对 MHC Ⅱ类缺陷小鼠进行疫苗接种,可以引发广泛的 CD8(+) T 细胞免疫反应。此外,诱导的反应赋予了针对高剂量侵袭性克隆 13 株 LCMV 攻击的显著细胞毒性 CD8(+) T 细胞介导的保护作用。相比之下,在缺乏 CD4(+) T 细胞的情况下,用编码不连接的 LCMV 糖蛋白的腺病毒进行疫苗接种会导致病毒控制减弱,并且小鼠可能因不完全保护而死于免疫病理学增加。在感染侵袭性较弱的 Traub 株后,任何接种疫苗的小鼠均未观察到急性死亡率。然而,LCMV Traub 感染导致未接种疫苗的 MHC Ⅱ类缺陷小鼠的晚期死亡率加速;在这种情况下,我们观察到接种疫苗的小鼠的死亡率延迟趋势很强,而与疫苗的性质无关。这些结果表明,即使在 Th 缺陷个体中,经过优化的疫苗接种也可能导致对急性病毒感染的有效保护,但这种免疫的持续时间是有限的。尽管如此,对于 CD4(+) T 细胞缺陷不完全或短暂的某些免疫缺陷,这些结果非常令人鼓舞。