Local T/B cooperation in inflamed tissues is supported by T follicular helper-like cells

Dana Vu Van, Katja C. Beier, Lea-Jean Pietzke, Maysun S. Al Baz, Randi K. Feist, Stephanie Gurka, Eckard Hamelmann, Richard A. Kroczek and Andreas Hutloff ()
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Dana Vu Van: Chronic Immune Reactions, German Rheumatism Research Centre, A Leibniz Institute
Katja C. Beier: Pediatric Pneumology and Immunology, Charité University Medicine
Lea-Jean Pietzke: Chronic Immune Reactions, German Rheumatism Research Centre, A Leibniz Institute
Maysun S. Al Baz: Chronic Immune Reactions, German Rheumatism Research Centre, A Leibniz Institute
Randi K. Feist: Chronic Immune Reactions, German Rheumatism Research Centre, A Leibniz Institute
Stephanie Gurka: Molecular Immunology, Robert Koch Institute
Eckard Hamelmann: Children’s Hospital of Ruhr University
Richard A. Kroczek: Molecular Immunology, Robert Koch Institute
Andreas Hutloff: Chronic Immune Reactions, German Rheumatism Research Centre, A Leibniz Institute

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract Autoimmune diseases and other inflammatory conditions are characterized by large lymphocytic tissue infiltrates in which T and B cells can be found in close contact. Here, using a murine airway inflammation model, we compare antigen-specific T and B cells in lung tissue versus lung-draining lymph node. In the lung we identify a B-cell population exhibiting a classical germinal centre phenotype without being organized into ectopic lymphoid tissue. By contrast, classical CXCR5+ Bcl-6+ T follicular helper cells are not present. Nevertheless, lung-infiltrating T cells exhibit follicular helper-like properties including the potential to provide help to naive B cells. The lung tissue is also a survival niche for memory T and B cells remaining in residual peribronchial infiltrates after resolution of inflammation. Collectively, this study shows the importance of T/B cooperation not only in lymph nodes but also in inflamed peripheral tissues for local antibody responses to infection and autoimmunity.

Date: 2016
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DOI: 10.1038/ncomms10875

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