Key Points Pathogen-specific TM are a prodigious source of chemokines. The chemokine-expression patterns of TM largely resemble those of TE. Unique TM chemokine signatures in acute/chronic infection are of diagnostic value. Pathogen-specific memory T cells (TM) contribute to enhanced immune protection under conditions of reinfection, and their effective recruitment into a recall response relies, in part, on cues imparted by chemokines that coordinate their spatiotemporal positioning. An integrated perspective, however, needs to consider TM as a potentially relevant chemokine source themselves. In this study, we employed a comprehensive transcriptional/translational profiling strategy to delineate the identities, expression patterns, and dynamic regulation of chemokines produced by murine pathogen-specific TM. CD8+TM, and to a lesser extent CD4+TM, are a prodigious source for six select chemokines (CCL1/3/4/5, CCL9/10, and XCL1) that collectively constitute a prominent and largely invariant signature across acute and chronic infections. Notably, constitutive CCL5 expression by CD8+TM serves as a unique functional imprint of prior antigenic experience; induced CCL1 production identifies highly polyfunctional CD8+ and CD4+TM subsets; long-term CD8+TM maintenance is associated with a pronounced increase of XCL1 production capacity; chemokines dominate the earliest stages of the CD8+TM recall response because of expeditious synthesis/secretion kinetics (CCL3/4/5) and low activation thresholds (CCL1/3/4/5/XCL1); and TM chemokine profiles modulated by persisting viral Ags exhibit both discrete functional deficits and a notable surplus. Nevertheless, recall responses and partial virus control in chronic infection appear little affected by the absence of major TM chemokines. Although specific contributions of TM-derived chemokines to enhanced immune protection therefore remain to be elucidated in other experimental scenarios, the ready visualization of TM chemokine-expression patterns permits a detailed stratification of TM functionalities that may be correlated with differentiation status, protective capacities, and potential fates.

中文翻译：

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病原体特异性 T 细胞的趋化因子特征 II：急性和慢性感染中的记忆 T 细胞

要点 病原体特异性 TM 是趋化因子的巨大来源。TM 的趋化因子表达模式在很大程度上类似于 TE 的趋化因子表达模式。急性/慢性感染中独特的 TM 趋化因子特征具有诊断价值。病原体特异性记忆 T 细胞 (TM) 有助于在再感染条件下增强免疫保护，并且它们有效地募集到回忆反应中部分依赖于协调其时空定位的趋化因子所传递的线索。然而，综合观点需要将 TM 本身视为潜在相关的趋化因子来源。在这项研究中，我们采用了全面的转录/翻译分析策略来描述由小鼠病原体特异性 TM 产生的趋化因子的特性、表达模式和动态调节。CD8+TM，以及在较小程度上的 CD4+TM，是六种选择趋化因子（CCL1/3/4/5、CCL9/10 和 XCL1）的巨大来源，它们共同构成了急性和慢性感染的突出且基本不变的特征。值得注意的是，CD8+TM 的组成型 CCL5 表达作为先前抗原经验的独特功能印记；诱导的 CCL1 产生鉴定了高度多功能的 CD8+ 和 CD4+TM 亚群；CD8+TM 的长期维护与 XCL1 生产能力的显着增加有关；由于快速合成/分泌动力学 (CCL3/4/5) 和低激活阈值 (CCL1/3/4/5/XCL1)，趋化因子在 CD8+TM 回忆反应的最早阶段占主导地位；和 TM 趋化因子谱调节的持续病毒 Ags 表现出离散的功能缺陷和显着的过剩。尽管如此，慢性感染中的回忆反应和部分病毒控制似乎不受主要 TM 趋化因子的影响。尽管 TM 衍生趋化因子对增强免疫保护的具体贡献因此在其他实验场景中仍有待阐明，但 TM 趋化因子表达模式的现成可视化允许对可能与分化状态、保护能力和潜在的命运。