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and Results in Cell Apoptosis Through TNF-1
* Graduate Institute of Biochemistry, Medical College, National Cheng Kung University, Tainan, Taiwan; and
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-
. 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- and induces
apoptosis.
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