Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Cell. 2012 Sep 14;150(6):1249-63. doi: 10.1016/j.cell.2012.08.015.
A defining feature of vertebrate immunity is the acquisition of immunological memory, which confers enhanced protection against pathogens by mechanisms that are incompletely understood. Here, we compared responses by virus-specific naive T cells (T(N)) and central memory T cells (T(CM)) to viral antigen challenge in lymph nodes (LNs). In steady-state LNs, both T cell subsets localized in the deep T cell area and interacted similarly with antigen-presenting dendritic cells. However, upon entry of lymph-borne virus, only T(CM) relocalized rapidly and efficiently toward the outermost LN regions in the medullary, interfollicular, and subcapsular areas where viral infection was initially confined. This rapid peripheralization was coordinated by a cascade of cytokines and chemokines, particularly ligands for T(CM)-expressed CXCR3. Consequently, in vivo recall responses to viral infection by CXCR3-deficient T(CM) were markedly compromised, indicating that early antigen detection afforded by intranodal chemokine guidance of T(CM) is essential for efficient antiviral memory.
脊椎动物免疫的一个显著特征是获得免疫记忆,通过机制不完全理解的机制增强对病原体的保护。在这里,我们比较了病毒特异性幼稚 T 细胞 (T(N)) 和中央记忆 T 细胞 (T(CM)) 对淋巴结 (LN) 中病毒抗原挑战的反应。在稳态 LN 中,两种 T 细胞亚群都定位于深 T 细胞区,并与抗原呈递树突状细胞以相似的方式相互作用。然而,当淋巴源性病毒进入时,只有 T(CM)迅速而有效地重新定位到 LN 最外层的皮质、滤泡间和被膜下区域,病毒感染最初局限于这些区域。这种快速的外周化是由一系列细胞因子和趋化因子协调的,特别是 T(CM)表达的 CXCR3 的配体。因此,CXCR3 缺陷型 T(CM)对病毒感染的体内回忆反应明显受损,表明通过 T(CM) 内节结趋化因子引导进行早期抗原检测对于有效的抗病毒记忆至关重要。