IFN-γ licenses CD11b(+) cells to induce progression of systemic lupus erythematosus

Shaabani, N. and Honke, N. and Dolff, S. and Gorg, B. and Khairnar, V. and Merches, K. and Duhan, V. and Metzger, S. and Recher, M. and Barthuber, C. and Hardt, C. and Proksch, P. and Haussinger, D. and Witzke, O. and Lang, P. A. and Lang, K. S.. (2015) IFN-γ licenses CD11b(+) cells to induce progression of systemic lupus erythematosus. Journal of Autoimmunity, 62. pp. 11-21.

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Official URL: https://edoc.unibas.ch/62409/

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Autoantibodies are a hallmark of autoimmune diseases, such as rheumatoid arthritis, autoimmune hepatitis, and systemic lupus erythematosus (SLE). High titers of anti-nuclear antibodies are used as surrogate marker for SLE, however their contribution to pathogenesis remains unclear. Using murine model of SLE and human samples, we studied the effect of immune stimulation on relapsing of SLE. Although autoantibodies bound to target cells in vivo, only additional activation of CD8(+) T cells converted this silent autoimmunity into overt disease. In mice as well as in humans CD8(+) T cells derived IFN-gamma enhanced expression of Fc-receptors on CD11b(+) cells. High expression of Fc-receptors allowed CD11b(+) cells to bind to antibody covered target cells and to destroy them in vivo. We found that autoantibodies induce clinically relevant disease when adaptive immunity, specific for disease non-related antigen, is activated.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Immunodeficiency (Recher)
UniBasel Contributors:Recher, Mike
Item Type:Article, refereed
Article Subtype:Research Article
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:19 Nov 2018 18:02
Deposited On:19 Nov 2018 18:02

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