Inflammation-induced formation of fat-associated lymphoid clusters.
Authors/Creators
- 1. School of Immunity and Infection, IBR-MRC Centre for Immune Regulation, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
- 2. MRC Laboratory of Molecular Biology, Cambridge, UK
- 3. [1] Inflammation Biology, German Rheumatism Research Center, Leibniz Institute, Berlin, Germany. [2] Engelhardt Institute of Molecular Biology, Moscow, Russia. [3] 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, UK.
- 6. College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK.
- 7. Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
- 8. [1] Division of Immunology, Biomedical Sciences Research Center 'Alexander Fleming', Vari, Greece. [2] Departament of Experimental Physiology, National and Kapodistrian University of Athens, Athens, Greece.
- 9. Lymphocyte Signalling and Development Programme, The Babraham Institute, Cambridge, UK.
- 10. [1] Inflammation Biology, German Rheumatism Research Center, Leibniz Institute, Berlin, Germany. [2] Engelhardt Institute of Molecular Biology, Moscow, Russia. [3] Lomonosov Moscow State University, Moscow, Russia.
- 11. MRC Laboratory of Molecular Biology, Cambridge, UK.
Description
Fat-associated lymphoid clusters (FALCs) are a type of lymphoid tissue associated with visceral fat. Here we found that the distribution of FALCs was heterogeneous, with the pericardium containing large numbers of these clusters. FALCs contributed to the retention of B-1 cells in the peritoneal cavity through high expression of the chemokine CXCL13, and they supported B cell proliferation and germinal center differentiation during peritoneal immunological challenges. FALC formation was induced by inflammation, which triggered the recruitment of myeloid cells that expressed tumor-necrosis factor (TNF) necessary for signaling via the TNF receptors in stromal cells. Natural killer T cells (NKT cells) restricted by the antigen-presenting molecule CD1d were likewise required for the inducible formation of FALCs. Thus, FALCs supported and coordinated the activation of innate B cells and T cells during serosal immune responses.
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