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46. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 32. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), Wissenschaftliche Herbsttagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR)

19.09. - 22.09.2018, Mannheim

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Adenosine A3-Rezeptor is upregulated in human SLE B cells

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  • Magdalena Siekierka-Harreis - Poliklinik, Funktionsbereich & Hiller Forschungszentrum für Rheumatologie, UKD, Heinrich-Heine-Universität, Rheumatologie, Düsseldorf
  • Merle Schallehn - Medizinische Fakultät, Heinrich-Heine Universität Düsseldorf, Rheumatologie, Poliklinik, Funktionsbereich & Hiller Forschungszentrum, Düsseldorf
  • Nadine Honke - Medizinisch Fakultät, Heinrich-Heine Universität, Rheumatologie, Poliklinik, Funktionsbereich & Hiller Forschungszentrum, Düsseldorf
  • Katharina Krebber - Medizinisch Fakultät, Heinrich-Heine Universität, Rheumatologie, Poliklinik, Funktionsbereich & Hiller Forschungszentrum, Düsseldorf
  • Dennis Bleck - Medizinisch Fakultät, Heinrich-Heine Universität, Rheumatologie, Poliklinik, Funktionsbereich & Hiller Forschungszentrum, Düsseldorf
  • Gamal Chehab - Poliklinik, Funktionsbereich & Hiller Forschungszentrum für Rheumatologie, UKD, Heinrich-Heine-Universität Düsseldorf, Düsseldorf
  • Jutta Richter - Poliklinik, Funktionsbereich & Hiller Forschungszentrum für Rheumatologie, UKD, Heinrich-Heine-Universität Düsseldorf, Düsseldorf
  • Matthias Schneider - Poliklinik, Funktionsbereich & Hiller Forschungszentrum für Rheumatologie, UKD, Heinrich-Heine-Universität Düsseldorf, Düsseldorf
  • Georg Pongratz - Universitätsklinikum Düsseldorf, Poliklinik, Funktionsbereich & Hiller Forschungszentrum für Rheumatologie, Düsseldorf

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 46. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 32. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), Wissenschaftliche Herbsttagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Mannheim, 19.-22.09.2018. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocER.21

doi: 10.3205/18dgrh100, urn:nbn:de:0183-18dgrh1001

Published: February 5, 2019

© 2019 Siekierka-Harreis et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Background: Systemic Lupus Erythematosus (SLE) is a chronic, multisystem autoimmune disorder with dysregulation in many parts of the immune cascade. Purinergic signalling is well known to regulate immune cell functions. Adenosine plays an important role in animal models and human pathogenesis of arthritis, sepsis, asthma, ischaemia, wound healing, inflammatory bowel disease and cancer. Adenosine acts via four cell surface receptors: A1R, A2AR, A2BR, and A3R and its role in SLE is poorly understood so far. The aim of the study was to characterize the surface distribution of the adenosine receptors in human B cells from SLE patients in comparison to healthy controls in order to further elucidate purinergic pathways in this disease.

Methods: Blood samples from SLE patients were collected from n=8 adult SLE patients attending the outpatients’ Rheumatology department of the Heinrich-Heine-University Hospital Düsseldorf. All patients included fulfilled the revised criteria of the American College of Rheumatology for SLE. B cell-depleting- or cyclophosphamide therapy during the last 12 months before blood sampling served as exclusion criteria. All subjects gave their informed consent and the study was approved by the local ethics committee. Blood samples from healthy subjects (HC, n=8) were obtained from anonymous blood donors of the Transfusion Unit of the University Hospital Düsseldorf. B cells were purified according to an established protocol by density gradient centrifugation and subsequent B Cell isolation. Adenosine receptors were quantified by RT-PCR.

Results: We analysed the expression of adenosine receptors A1R, A2AR, A2BR and A3R by quantitative RT-PCR. Transcripts of all four adenosine receptors were detected in SLE and healthy B cells but only A3R expression was significantly increased in SLE B cells (n=8, p =0,049).

Conclusion: Adenosine signalling might be altered in human SLE B cells in comparison to HC as the A3R shows a different expression in SLE patients. As the A3 receptor signalling is known to be involved in immune cell proliferation and chemotaxis, further experiments are needed to specify its specific role in SLE B cells with the purpose to explore, whether adenosine signalling might represent a novel therapeutic target in SLE in the future.