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Abstract Number: 888

Plasma Cells Express the Novel Cytokine Interleukin-36α in Psoriatic and Rheumatoid Arthritis Synovium

Anja Derer1, Silke Frey2, Maria-Elena Messbacher2, Serena Bugatti3, Dominique L. Baeten4, Carlomaurizio Montecucco5, Georg A. Schett1 and Axel J. Hueber6, 1Dept of Medicine 3, Rheumatology and Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, 2Internal Medicine 3, University of Erlangen, Erlangen, Germany, 3Rheumatology and Translational Immunology Research Laboratories (LaRIT), Division of Rheumatology, IRCCS Policlinico S.Matteo Foundation/University of Pavia, Pavia, Italy, 4Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands, 5Division of Rheumatology, University of Pavia School of Medicine, IRCCS Policlinico San Matteo Foundation, Pavia, Italy, 6Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: interleukins (IL)

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Session Information

Title: Cytokines, Mediators, and Gene Regulation

Session Type: Abstract Submissions (ACR)

Background/Purpose: IL-36α is a recent described IL-1 cytokine family member with proinflammatory and clear pathogenic properties in psoriasis. Aim of this study was to determine IL-36α expression in psoriatic arthritis (PsA) compared to rheumatoid (RA) and osteoarthritis (OA).

Methods: Synovial tissue gathered from arthritis patients were stained for IL-36α, IL-36 receptor (IL-36R) and IL-36R antagonist (IL-36Ra) by immunohistochemistry and immunofluorescence. Lysates were tested for IL-36α by western blot analysis. Synovial fibroblasts (FLS) stimulated with IL-36α were assessed for cytokine expression.

Results: The IL-36R and its ligands IL-36α and IL-36Ra could be detected in inflammatory arthritis in the synovial lining layer as well as cellular infiltrates. IL-36α was significantly higher expressed in PsA and RA synovium compared to OA (p=0.0011 and p<0.0001, respectively). No differences were seen in IL-36R and IL-36Ra. The expression of IL-36α was confirmed by western blot analysis. IL-36α induced expression of IL-6 and IL-8 in FLS. CD138-positive plasma cells were determined as major cellular source for IL-36α.

Conclusion: We described that the novel cytokine IL-36α is upregulated in PsA and RA synovium mainly expressed by plasma cells. This insight needs further studies to determine if the IL-36 family can function as a potential target for arthritis therapy.


Disclosure:

A. Derer,
None;

S. Frey,
None;

M. E. Messbacher,
None;

S. Bugatti,
None;

D. L. Baeten,
None;

C. Montecucco,
None;

G. A. Schett,
None;

A. J. Hueber,
None.

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