Loss of IL-22 inhibits autoantibody formation in collagen-induced arthritis in mice

Odilia Corneth, Rogier Reijmers, Anne-Marie Otten - Mus, Patrick Asmawidjaja, Jan piet Hamburg, Natalie Papazian, Jurre Siegers, F Mourcin, R Amin, K Tarte, Rudi Hendriks, Tom Cupedo, Erik Lubberts

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Interleukin 22 (IL-22) expression is associated with increased joint destruction and disease progression in rheumatoid arthritis (RA). Although IL-22 is considered a proinflammatory cytokine, its mechanism of action in RA remains incompletely understood. Here, we used the collagen-induced arthritis model in IL-22 deficient (IL-22(-/-)) mice to study the role of IL-22 in RA. In spite of normal disease incidence, disease severity is significantly diminished in IL-22(-/-) mice. Moreover, pathogenicity of Th17 cells and development and function of B cells are unaffected. In contrast, splenic plasma cells, as well as serum autoantibody titers, are reduced in the absence of IL-22. At the peak of disease, germinal centers (GCs) are severely reduced in the spleens of IL-22(-/-) mice, correlating with a decline in GC B-cell numbers. Within the GC, we identified IL-22R1 expressing follicular dendritic cell-like stromal cells. Human lymphoid stromal cells respond to IL-22 ex vivo by inducing transcription of CXCL12 and CXCL13. We therefore postulate IL-22 as an important enhancer of the GC reaction, maintaining chemokine levels for the persistence of GC reactions, essential for the production of autoantibody-secreting plasma cells. Blocking IL-22 might therefore prevent immune-complex deposition and destruction of joints in RA patients.
Original languageUndefined/Unknown
Pages (from-to)1404-1414
Number of pages11
JournalEuropean Journal of Immunology
Issue number6
Publication statusPublished - 2016

Research programs

  • EMC MM-02-41-04
  • EMC MM-04-42-02
  • EMC MUSC-01-31-01

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