| First Author | Corneth OB | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 6 | Pages | 1404-14 |
| PubMed ID | 27067635 | Mgi Jnum | J:246947 |
| Mgi Id | MGI:5924368 | Doi | 10.1002/eji.201546241 |
| Citation | Corneth OB, et al. (2016) Loss of IL-22 inhibits autoantibody formation in collagen-induced arthritis in mice. Eur J Immunol 46(6):1404-14 |
| abstractText | Interleukin 22 (IL-22) expression is associated with increased joint destruction and disease progression in rheumatoid arthritis (RA). Although IL-22 is considered a pro-inflammatory 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. |
