J Immunol 2002 Oct 15;169(8):4288-97
Liao YC, Liang WG, Chen FW, Hsu JH, Yang JJ, Chang MS.
Graduate Institute of Biochemistry, Medical College, National Cheng Kung University, Tainan, Taiwan. 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.