Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA.
J Immunol. 2011 Jun 15;186(12):6667-71. doi: 10.4049/jimmunol.1004022. Epub 2011 May 13.
Effective vaccines against intracellular pathogens rely on the generation and maintenance of memory CD8 T cells (T(mem)). Hitherto, evidence has indicated that CD8 T(mem) use the common γ-chain cytokine IL-15 for their steady-state maintenance in the absence of Ag. This evidence, however, has been amassed predominantly from models of acute, systemic infections. Given that the route of infection can have significant impact on the quantity and quality of the resultant T(mem), reliance on limited models of infection may restrict our understanding of long-term CD8 T(mem) survival. In this article, we show IL-15-independent generation, maintenance, and function of CD8 T(mem) after respiratory infection with influenza virus. Importantly, we demonstrate that alternating between mucosal and systemic deliveries of the identical virus prompts this change in IL-15 dependence, necessitating a re-evaluation of the current model of CD8 T(mem) maintenance.
针对细胞内病原体的有效疫苗依赖于记忆 CD8 T 细胞（T(mem)）的产生和维持。迄今为止，有证据表明，在没有抗原的情况下，CD8 T(mem) 利用共同 γ 链细胞因子 IL-15 来维持其稳态。然而，这些证据主要来自于急性、系统性感染的模型。鉴于感染途径可能对产生的 T(mem) 的数量和质量产生重大影响，因此依赖于有限的感染模型可能会限制我们对长期 CD8 T(mem) 存活的理解。在本文中，我们显示了在流感病毒呼吸道感染后，CD8 T(mem) 的产生、维持和功能是不依赖于 IL-15 的。重要的是，我们证明了在相同病毒的黏膜和系统递送上交替进行，可以促使这种对 IL-15 依赖性的改变，这需要重新评估当前的 CD8 T(mem) 维持模型。
