The Journal of Experimental Medicine
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Published online 11 September 2006 doi:10.1084/jem.20061297
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 10, 2329-2338
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ARTICLE

 Essential roles of DC-derived IL-15 as a mediator of inflammatory responses in vivo

Toshiaki Ohteki1, Hiroyuki Tada1, Kazuto Ishida1, Taku Sato1, Chikako Maki2, Taketo Yamada3, Junji Hamuro2, and Shigeo Koyasu2,4

1 Department of Immunology, Akita University School of Medicine, Akita 010-8543, Japan
2 Department of Microbiology and Immunology and 3 Department of Pathology, Keio University School of Medicine, Tokyo 160-8582, Japan
4 Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan

CORRESPONDENCE Toshiaki Ohteki: tohteki{at}med.akita-u.ac.jp

Interleukin (IL)-15 is expressed in a variety of inflammatory diseases. However, the contribution of dendritic cell (DC)–derived IL-15 to the development of diseases is uncertain. Using established models of Propionibacterium acnes (P. acnes)– and zymosan-induced liver inflammation, we observed granuloma formation in the livers of wild-type (WT) and RAG-2–/– mice but not in those of IL-15–/– mice. We demonstrate that this is likely caused by an impaired sequential induction of IL-12, IFN-{gamma}, and chemokines necessary for monocyte migration. Likewise, lethal endotoxin shock was not induced in P. acnes– and zymosan-primed IL-15–/– mice or in WT mice treated with a new IL-15–neutralizing antibody. In both systems, proinflammatory cytokine production was impaired. Surprisingly, neither granuloma formation, lethal endotoxin shock, nor IL-15 production was induced in mice deficient for DCs, and adoptive transfer of WT but not IL-15–/– DCs restored the disease development in IL-15–/– mice. Collectively, these data indicate the importance of DC-derived IL-15 as a mediator of inflammatory responses in vivo.

Abbreviations used: BMDC, BM-derived DC; DAB, 3,3'-diaminobenzidine; DTR, diphtheria toxin receptor; DTR tg, CD11c-DTR-GFP transgenic; GOT and GPT, glutamic-oxaloacetic and -pyruvic transaminase, respectively; GSH, glutathione; H&E, hematoxylin and eosin; HRP, horseradish peroxidase; RA, rheumatoid arthritis.

T. Ohteki and H. Tada contributed equally to this work.


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