Publikation
Type I interferon signaling in fibroblastic reticular cells prevents exhaustive activation of antiviral CD8 T cells
Wissenschaftlicher Artikel/Review - 11.09.2020
Pérez Shibayama Christian Ivan, Gil Cruz Cristina, Colston Julia, Novkovic Mario, De Martin Angelina, Ring Sandra, Onder Lucas, Cheng Hung-Wei, Lütge Mechthild, Islander Ulrika, Ludewig Burkhard
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Abstract: http://immunology.sciencemag.org/cgi/content/abstract/5/51/eabb7066?ijkey=SVyn0z7cc6os.&keytype=ref&siteid=immunology
Reprint: http://immunology.sciencemag.org?ijkey=SVyn0z7cc6os.&keytype=ref&siteid=immunology
Full text: http://immunology.sciencemag.org/cgi/content/full/5/51/eabb7066?ijkey=SVyn0z7cc6os.&keytype=ref&siteid=immunology
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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 () 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.