作者：Ja Shugart，S Bambina，AF Alice，R Montler，KS Bahjat
动物
记忆性CD8+T细胞快速增殖和获得溶细胞活性是保护细胞内病原体免疫的关键。控制这一召回反应的信号仍不清楚。提示当全身炎症受*，记忆CD8+T细胞自身产生CD40L是二次扩张的重要催化剂。二次免疫同时伴有高水平的全身炎症，导致CD8+T细胞继发增殖，独立于CD4+T细胞和CD40-CD40L信号。相反，当炎症反应受*，记忆中CD8+T细胞的二次扩张需要产生CD40L的细胞，而记忆的CD8+T细胞可以提供这一信号。这些结果表明，免疫接种方案对CD40L表达的CD8+T细胞的依赖性不同，提示CD8+T细胞的CD40L表达是一种在炎症受*促进记忆性CD8+T细胞二次扩增的有效机制。
小鼠静脉注射单核细胞增多症。取脾脏和肝脏在Omni Prep多样本匀浆器上进行匀浆.均质被镀以进行菌落计数。
Authors: JA Shugart, S Bambina, AF Alice, R Montler, KS Bahjat
Animal
The ability of memory CD8+ T cells to rapidly proliferate and acquire cytolytic activity is critical for protective immunity against intracellular pathogens. The signals that control this recall response remain unclear. We show that CD40L production by memory CD8+ T cells themselves is an essential catalyst for secondary expansion when systemic inflammation is limited. Secondary immunization accompanied by high levels of systemic inflammation results in CD8+ T cell secondary expansion independent of CD4+ T cells and CD40-CD40L signaling. Conversely, when the inflammatory response is limited, memory CD8+ T cell secondary expansion requires CD40L-producing cells, and memory CD8+ T cells can provide this signal. These results demonstrate that vaccination regimens differ in their dependence on CD40L-expressing CD8+ T cells for secondary expansion, and propose that CD40L-expression by CD8+ T cells is a fail-safe mechanism that can promote memory CD8+ T cell secondary expansion when inflammation is limited.
Mice were challenged with L. monocytogenes intravenously. Spleens and livers were harvested and homogenized on an Omni Prep multi-sample homogenizer. Homogenates were plated for colony enumeration.
