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T cell specific Cxcr5deficiency preventsrheumatoid arthritis Georgios L. MoschovakisAnja BubkeMichaela Friedrichsen2017 год

T cell specific Cxcr5 deficiency prevents rheumatoid arthritis
статья из журнала

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Аннотация: The chemokine receptor CXCR5 is primarily expressed on B cells and Tfh cells and facilitates their migration towards B cell follicles. In the present study we investigated the role of the CXCL13/CXCR5 axis in the pathogenesis of rheumatoid arthritis (RA) and specifically addressed the impact of CXCR5-mediated T and B cell migration in this disease. Employing collagen-induced arthritis (CIA) we identify CXCR5 as an absolutely essential factor for the induction of inflammatory autoimmune arthritis. Cxcr5-deficient mice and mice selectively lacking Cxcr5 on T cells were completely resistant to CIA, showed impaired germinal center responses and failed to mount an IgG1 antibody response to collagen II. Selective ablation of CXCR5 expression in B cells also led to suppression of CIA owing to diminished GC responses in secondary lymphoid organs (SLO) and impaired anti-collagen II antibody production. Chimeric mice harboring Cxcr5-proficient and Cxcr5-deficient immune cells revealed SLO and not the synovial tissue as the compartment where CXCR5-mediated cell migration induces autoimmune inflammation in arthritis. Thus our data demonstrate that CXCR5-mediated co-localization of Tfh cells and B cells in SLOs is absolutely essential for the induction of RA and identify CXCR5 and Tfh cells as promising therapeutic targets for the treatment of RA.
Год издания: 2017
Авторы: Georgios L. Moschovakis, Anja Bubke, Michaela Friedrichsen, Christine S. Falk, Regina Feederle, Reinhold Förster
Издательство: Nature Portfolio
Источник: Scientific Reports
Ключевые слова: T-cell and B-cell Immunology, Chemokine receptors and signaling, Immunotherapy and Immune Responses
Другие ссылки: Scientific Reports (PDF)
Scientific Reports (HTML)
DOAJ (DOAJ: Directory of Open Access Journals) (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
PubMed (HTML)