Inflammation-induced formation of fat-associated lymphoid clusters
Authors/Creators
- Cécile Bénézech1
- Nguyet-Thin Luu1
- Jennifer A. Walker2
- Andrei A. Kruglov3
- Yunhua Loo4
- Kyoko Nakamura1
- Yang Zhang1
- Saba Nayar1
- Lucy H. Jones5
- Adriana Flores-Langarica1
- Alistair McIntosh1
- Jennifer Marshall1
- Francesca Barone1
- Gurdyal Besra6
- Katherine Miles7
- Judith E. Allen5
- Mohini Gray7
- George Kollias8
- Adam F. Cunningham1
- David R. Withers1
- Kai Michael Toellner1
- Nick D. Jones1
- Marc Veldhoen4
- Sergei A. Nedospasov3
- Andrew N.J. McKenzie2
- Jorge H. Caamaño11
- 1. School of Immunity and Infection, IBR-MRC Centre for Immune Regulation, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK
- 2. MRC Laboratory of Molecular Biology, Cambridge, UK
- 3. German Rheumatism Research Center, Berlin, Germany; Engelhardt Institute of Molecular Biology, Moscow, Russia; Lomonosov Moscow State University, Moscow, Russia
- 4. Lymphocyte Signalling and Development Programme, The Babraham Institute, Cambridge, UK
- 5. Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh
- 6. College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK
- 7. Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK
- 8. Fleming Institute, Athens, Greece
Description
Fat-associated lymphoid clusters (FALCs) are a recently discovered type of lymphoid tissue associated with visceral fat. Here we show that distribution of FALCs was heterogeneous with the pericardium containing large numbers of these clusters. FALCs contributed to the retention of B-1 B cells in the peritoneal cavity through high expression of the chemokine CXCL13 and supported B cell proliferation and germinal center differentiation during peritoneal immune challenges. FALC formation was induced by inflammation, which triggered recruitment of myeloid cells that express tumor necrosis factor (TNF) necessary for TNF receptor-signaling in stromal cells. CD1drestricted Natural killer T (NKT) cells were likewise required for inducible formation of FALCs. Thus, FALCs support and coordinate innate B and T cell activation during serosal immune responses.
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