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The Journal of Immunology, 2002, 169: 4288-4297.
Copyright © 2002 by The American Association of Immunologists

IL-19 Induces Production of IL-6 and TNF-{alpha} and Results in Cell Apoptosis Through TNF-{alpha}1

Yuan-Chun Liao*, Wei-Guang Liang*, Feng-Wei Chen*, Ju-Hui Hsu{dagger}, Jiann-Jou Yang{dagger} and Ming-Shi Chang2,*,{dagger}

* Graduate Institute of Biochemistry, Medical College, National Cheng Kung University, Tainan, Taiwan; and {dagger} Chi-Mei Medical Center, Tainan, Taiwan

IL-10 is an immunosuppressive cytokine in the immune system. It was in clinical trail as an anti-inflammatory therapy for inflammatory bowel disease and various autoimmune diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. IL-19 belongs to the IL-10 family, which includes IL-10, IL-19, IL-20, IL-22, melanoma differentiation-associated gene (MDA-7, IL-24), and AK155 (IL-26). Despite a partial homology in their amino acid sequences, they are dissimilar in their biologic functions. Little is known about the biologic function and gene regulation of IL-19. To understand the gene regulation of human IL-19, we identified a human IL-19 genomic clone and analyzed its promoter region. Five fusion genes containing different regions upstream of exon 1 linked to a luciferase reporter gene were expressed in the canine kidney epithelial-like Madin-Darby canine kidney cells. A fusion gene containing 394 bp showed luciferase activity 7- to 8-fold higher than the negative control of the promoterless fusion gene. We also isolated a full-length mouse cDNA clone. Mouse IL-19 shared 71% amino acid identity with human IL-19. Treatment of monocytes with mouse IL-19 induced the production of IL-6 and TNF-{alpha}. It also induced mouse monocyte apoptosis and the production of reactive oxygen species. Taken together, our results indicate that mouse IL-19 may play some important roles in inflammatory responses because it up-regulates IL-6 and TNF-{alpha} and induces apoptosis.




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