Follicular dendritic cells emerge from ubiquitous perivascular precursors |
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Authors: | Nike Julia Krautler Veronika Kana Jan Kranich Yinghua Tian Dushan Perera Doreen Lemm Petra Schwarz Annika Armulik Jeffrey L Browning Michelle Tallquist Thorsten Buch José B Oliveira-Martins Caihong Zhu Mario Hermann Ulrich Wagner Robert Brink Mathias Heikenwalder Adriano Aguzzi |
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Affiliation: | 1 Institute of Neuropathology, University Hospital of Zurich, 8091 Zurich, Switzerland 2 Division of Visceral and Transplant Surgery, University Hospital of Zurich, 8091 Zurich, Switzerland 3 Garvan Institute of Medical Research, Darlinghurst, New South Wales, Sydney 2010, Australia 4 Biogen Idec, Immunobiology, 124 Cambridge Center, Cambridge, MA 02142, USA 5 UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9148, USA 6 Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland 7 Institute of Laboratory Animal Science, University of Zurich, 8057 Zurich, Switzerland 8 Ludwig Institute for Cancer Research, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA |
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Abstract: | The differentiation of follicular dendritic cells (FDC) is essential to the remarkable microanatomic plasticity of lymphoid follicles. Here we show that FDC arise from ubiquitous perivascular precursors (preFDC) expressing platelet-derived growth factor receptor β (PDGFRβ). PDGFRβ-Cre-driven reporter gene recombination resulted in FDC labeling, whereas conditional ablation of PDGFRβ(+)-derived cells abolished FDC, indicating that FDC originate from PDGFRβ(+) cells. Lymphotoxin-α-overexpressing prion protein (PrP)(+) kidneys developed PrP(+) FDC after transplantation into PrP(-) mice, confirming that preFDC exist outside lymphoid organs. Adipose tissue-derived PDGFRβ(+) stromal-vascular cells responded to FDC maturation factors and, when transplanted into lymphotoxin β receptor (LTβR)(-) kidney capsules, differentiated into Mfge8(+)CD21/35(+)FcγRIIβ(+)PrP(+) FDC capable of trapping immune complexes and recruiting B cells. Spleens of lymphocyte-deficient mice contained perivascular PDGFRβ(+) FDC precursors whose expansion required both lymphoid tissue inducer (LTi) cells and lymphotoxin. The ubiquity of preFDC and their strategic location at blood vessels may explain the de novo generation of organized lymphoid tissue at sites of lymphocytic inflammation. |
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