gms | German Medical Science

43. Kongress der Deutschen Gesellschaft für Rheumatologie, 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 25. Wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

02.-05. September 2015, Bremen

Beta-2 adrenoceptor signal is augmented in B cells in the course of arthritis to increase IL-10

Meeting Abstract

  • Georg Pongratz - Universitätsklinikum Regensburg, Klinik und Poliklinik für Innere Medizin I, Regensburg
  • Clemens Wiest - Universitätsklinikum Regensburg, Regensburg
  • Madlen Melzer - Universitätsklinikum Regensburg, Regensburg
  • Rainer H. Straub - Innere Med I, Universitätsklinikum Regensburg, Regensburg

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 43. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 25. wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Bremen, 02.-05.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc52.07 - ER.06

doi: 10.3205/15dgrh048, urn:nbn:de:0183-15dgrh0483

Published: September 1, 2015

© 2015 Pongratz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Introduction: Splenic B cells from collagen-induced arthritis (CIA) mice react to a β2-adrenoceptor (AR) stimulus with increased IL-10 production and adoptive transfer of these cells decreases disease activity. However, B cells from unimmunized mice do not adequately increase IL-10. Therefore, we test the hypothesis that sensitivity to catecholamines changes during CIA. Furthermore, we wanted to test if human peripheral blood B cells from osteoarthritis (OA) and rheumatoid arthritis (RA) patients also increase IL-10 following a β2-adrenergic stimulus.

Methods: FACS, ELISA, human and mouse B cell culture, CIA

Results: In the course of CIA the percentage of β2-AR+ B cells increased (ANOVA p<0.05). Mean fluorescence intensity (MFI) for G-protein coupled receptor kinase (GRK2) decreased from day 6 p.i. (ANOVA p<0.0001). The relative increase in phosphorylation of p38 (ANOVA p<0.001) and cAMP responsive element binding protein (CREB, ANOVA p<0.001) following a β2-AR stimulus is augmented in late CIA. In human B cells, similar mechanisms are in place, because β2-AR stimulation of RA but not OA B cells increased IL-10.

Conclusion: The current data show that B cells become more sensitive to β2-AR stimuli in the course of CIA, possibly due to a decrease in GRK2 and increase in the percentage of β2AR expressing splenic B cells. Increased catecholamine sensitivity might support B cell and IL-10 mediated anti-inflammatory mechanisms in the late phase of CIA. A similar mechanim is observed in human peripheral B cells and might be used to improve treatment of autoimmune arthritis.