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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

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IL-17-producing ©™T cells are important for the development of arthritis in a rheumatoid arthritis model

Aoi Akitsu12*, Harumichi Ishigame1, Shigeru Kakuta1, Shinobu Saijo1 and Yoichiro Iwakura12

  • * Corresponding author: Aoi Akitsu

Author Affiliations

1 Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Japan

2 Japan Society for the Promotion of Science (JSPS) 3Core Research for Evolutional Science and Technology (CREST), Japan

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Arthritis Research & Therapy 2012, 14(Suppl 1):P3  doi:10.1186/ar3604

The electronic version of this article is the complete one and can be found online at:

Published:9 February 2012

© 2012 Akitsu et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


IL-1 receptor antagonist deficient (Il1rn-/-) mice spontaneously develop arthritis. We previously demonstrated that IL-17 plays a crucial role in the development of arthritis in Il1rn-/- mice. Furthermore we showed that IL-1 Ra-deficiency in T cells is important for the development of arthritis. It is not known, however, which IL-17-producing cells are involved in the pathogenesis of arthritis in this model.


To identify the source of IL-17 in Il1rn-/- mice, we analyzed IL-17-producing cells. We found that IL-17 production from both CD4+ T cells and ©™T cells was increased in the draining lymph nodes. To clarify the roles of CD4+ T cells and ©™T cells in the development of arthritis, ©™T cells or CD4+ T cells were depleted in Il1rn-/- mice using antibodies. The development of disease was suppressed in both cases, suggesting both Th17 cells and IL-17-producing ©™T cells were involved in the pathogenesis. Then, the pathogenic role of IL-17-producing ©™T cells in the absence of Th17 cells was examined.

We generated mice with IL-17 producing ©™T cells, but without Th17 cells, by adoptively transferring Il17-/-Il1rn-/--T cells into nude mice in which IL-17-producing ©™T cells are present. We found that these mice still developed arthritis and that only ©™T cells produced IL-17. Finally, to corroborate that the development of arthritis in this transfer system is dependent on IL-17, we adoptively transferred Il17-/-Il1rn-/--T cells into Il17-/-nu/nu mice. The development of arthritis was significantly suppressed in Il17-/-Il1rn-/--T cell-transferred Il17-/-nu/nu mice compared with Il-17+/+nu/nu mice transferred with Il17-/-Il1rn-/--T cells, suggesting that ©™T -cell-derived IL-17 is important for the develop arthritis.


These results indicate that ©™T cell-derived IL-17 plays an important role in the pathogenesis of arthritis in Il1rn-/- mice.