Dr Dagmar Scheel-Toellner PhD

Image of Dagmar Scheel-Toellner

Institute of Inflammation and Ageing
Professor of Inflammation Research

Contact details

Rheumatology Research Group
Institute of Inflammation and Ageing
College of Medical and Dental Sciences
University of Birmingham
B15 2TT

Dagmar Scheel-Toellner leads a research team that investigates the basic mechanism of joint inflammation in patients with rheumatoid arthritis. She initially trained as a pharmacist, and the translation of her research on autoimmunity into therapeutic strategies is still an important long-term aim in her work. She closely collaborates with her clinical colleagues within the Rheumatology Research Group in their investigation of the early stages of the development of rheumatoid arthritis. Currently, a major focus of her work is the investigation of a novel proinflammatory B cell subset her team has identified in the joints of patients with rheumatoid arthritis. Dagmar has published widely on the regulation of apoptosis and the cell-cytokine network in inflammatory disease. Currently, most of the work in her team is funded by the MRC, Arthritis Research UK, and the EU.


  • Member of the Higher Education Academy, 2003
  • PhD (Dr rer. nat.) in Immunology and Pharmaceutical Biology, Christian Albrechts University, Kiel, 1994
  • State examination in Pharmacy, (Equivalent of BSc) Christian Albrechts University, Kiel, Germany, 1989


Dagmar Scheel-Toellner qualified as a pharmacist from the Christian-Albrechts University in Kiel, Germany in 1989. She went on to study for a PhD in the Department of Immunology and Cell Biology at the Research Centre Borstel with Professor Johannes Gerdes. In 1994 she was awarded the title Dr. rer. nat. (equivalent to PhD in Natural Sciences) by the Christian Albrechts University, Kiel for the thesis: “Investigation of the expression of CD26 in granulomatous tissue and normal peripheral blood.” with the grade “summa cum laude”. (Excellent)

In 1994 Dagmar moved to Birmingham to join the Department of Rheumatology as a post-doctoral research fellow with Mike Salmon and from 1996 also with Janet Lord.

She was awarded a Non-clinical Career Development Fellowship by  Arthritis Research UK in 2004. In the following years she established her research team and was promoted to Senior Research Fellow in 2007.

The Career Development Fellowship was followed by an Arthritis Research UK funded Career Progression Fellowship leading to a substantive post in the School of Immunity and Infection in 2010.

In 2015 Dagmar was promoted to Reader in Translational Inflammation Research.


Teaching Programmes

Postgraduate supervision

Dagmar is currently supervising several PhD students working on basic disease mechanisms in rheumatoid arthritis. 

If you are interesting in studying is this subject area please contact Dagmar on the contact details above, or for any general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings.   


Joint damage in patients with rheumatoid arthritis (RA) is driven by a complex network of interactions between resident stromal cells and infiltrating inflammatory cells. Within this network, signals are exchanged via cell-surface interactions and soluble factors such as cytokines and hormones. Dagmar’s group, in collaboration with other members of the Rheumatology Research Group, uses a systematic approach to detect cytokine gene expression in isolated inflammatory cell populations to establish an overview of the inflammatory network in the joint of patients with RA.

Current projects within Dagmar’s team include:

  • The role of a novel proinflammatory B cell population in RA
  • Characterisation of cytokine profiles in synovial tissue and in sorted inflammatory cell populations from rheumatoid synovial fluid
  • The role of neutrophils as producers of autoantigens in rheumatoid arthritis

All of these projects are directed at the identification of new targets and strategies for the treatment of Rheumatoid Arthritis.


Juarez M, McGettrick HM, Scheel-Toellner D, Yeo L, Spengler J, de Paz B, Hardy R, Cooper M, Raza K, Buckley CD and Filer A (2016) DKK1 expression by synovial fibroblasts in very early rheumatoid arthritis associates with lymphocyte adhesion in an in vitro flow co-culture system. Arthritis Res Ther 18:14

Lugonja B, Yeo L, Milward MR, Smith D, Dietrich T, Chapple IL, Rauz S, Williams GP, Barone F, de Pablo P, Buckley C, Hamburger J, Richards A, Poveda-Gallego A, Scheel-Toellner D and Bowman SJ (2016) Periodontitis prevalence and serum antibody reactivity to periodontal bacteria in primary Sjögren's syndrome: a pilot study. J Clin Periodontol 43(1):26-33

Spengler J, Lugonja B, Ytterberg AJ, Zubarev RA, Creese AJ, Pearson MJ, Grant MM, Milward M, Lundberg K, Buckley CD, Filer A, Raza K, Cooper PR, Chapple IL and Scheel-Toellner D (2015) Release of active Peptidyl Arginine Deiminase by neurotrophils can explain production of extracellular citrullinated autoantigens in Rheumatoid Arthritis synovial fluid. Arthritis Rheumatol 67(12):3135-45

Nanus DE, Filer AD, Yeo L, Scheel-Toellner D, Hardy R, Lavery GG, Stewart PM, Buckley CD, Tomlinson JW, Cooper MS and Raza K (2015) Differential glucocorticoid metabolism in patients with persistent versus resolving inflammatory arthritis. Arthritis Res Ther 17(1):121

Yeo L, Adlard N, Biehl M, Juarez M, Smallie T, Snow M, Buckley CD, Raza K, Filer A and Scheel-Toellner D (2016) Expression of chemokines CXCL4 and CXCL7 by synovial macrophages defines an early stage of rheumatoid arthritis. Ann Rheum Dis 75(4):763-71

Filer A, Antczak P, Parsonage GN, Legault HM, O'Toole M, Pearson MJ, Scheel-Toellner D, Raza K, Buckley CD and Falciani F (2015) Stromal transcriptional profiles reveal hierarchies of anatomical site, serum response and disease and identify disease specific pathways. PLoS One 10(3):e0120917

Yeo L, Lom H, Juarez M, Snow M, Buckley CD, Filer A, Raza K and Scheel-Toellner D (2015) Expression of FcRL4 defines a pro-inflammatory, RANKL-producing B cell subset in rheumatoid arthritis. Ann Rheum Dis 74(5):928-35
Highlighted in Nature Reviews in Rheumatology

Boumans MJ, Thurlings RM, Yeo L, Scheel-Toellner D, Vos K, Gerlag DM and Tak PP (2012) Rituximab abrogates joint destruction in rheumatoid arthritis by inhibiting osteoclastogenesis. Ann Rheum Dis 71(1):108-13

Hidalgo E, Essex SJ, Yeo L, Curnow SJ, Filer A, Cooper MS, Thomas AM, McGettrick HM, Salmon M, Buckley CD, Raza K and Scheel-Toellner D (2011) The response of T cells to IL-6 is differentially regulated by the microenvironment of the rheumatoid synovial fluid and tissue. Arthritis Rheum 63(11):3284-93

Yeo L, Toellner KM, Salmon M, Filer A, Buckley CD, Raza K and Scheel-Toellner D (2011) Cytokine mRNA profiling identifies B cells as a major source of RANKL in rheumatoid arthritis. Ann Rheum Dis 70(11):2022-8
Recommended in F1000, Highlighted in Nature Reviews in Rheumatology

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