Fibroblastic reticular cells (FRCs) are stromal cells that actively promote the induction of immune responses by coordinating the interaction of innate and adaptive immune cells. However, whether and to which extent immune cell activation is determined by lymph node FRC reprogramming during acute viral infection has remained unexplored. Here, we genetically ablated expression of the type I interferon-α receptor (Ifnar) in Ccl19-Cre⁺ cells and found that sensing of type I interferon imprints an antiviral state in FRCs and thereby preserves myeloid cell composition in lymph nodes of naive mice. During localized lymphocytic choriomeningitis virus infection, IFNAR signaling precipitated profound phenotypic adaptation of all FRC subsets enhancing antigen presentation, chemokine-driven immune cell recruitment, and immune regulation. The IFNAR-dependent shift of all FRC subsets toward an immunostimulatory state reduced exhaustive CD8⁺ T cell activation. In sum, these results unveil intricate circuits underlying type I IFN sensing in lymph node FRCs that enable protective antiviral immunity.

成纤维网状细胞 (FRC) 是基质细胞，通过协调先天性和适应性免疫细胞的相互作用，积极促进免疫反应的诱导。然而，免疫细胞激活是否以及在何种程度上由急性病毒感染期间的淋巴结 FRC 重编程决定仍然未探索。在这里，我们基因消除了 Ccl19-Cre ^{+ 中}I 型干扰素-α 受体 ( Ifnar ) 的表达细胞并发现 I 型干扰素的感知在 FRC 中留下了抗病毒状态，从而保留了幼稚小鼠淋巴结中的髓细胞组成。在局部淋巴细胞脉络丛脑膜炎病毒感染期间，IFNAR 信号传导促进了所有 FRC 亚群的深刻表型适应，增强了抗原呈递、趋化因子驱动的免疫细胞募集和免疫调节。所有 FRC 亚群向免疫刺激状态的 IFNAR 依赖性转变减少了彻底的 CD8 ⁺ T 细胞活化。总之，这些结果揭示了淋巴结 FRC 中 I 型 IFN 感应的复杂电路，这些电路能够实现保护性抗病毒免疫。