Details

Autor(en) / Beteiligte

• Liao, Yuan-Chun
• Liang, Wei-Guang
• Chen, Feng-Wei
• Hsu, Ju-Hui
• Yang, Jiann-Jou
• Chang, Ming-Shi

Titel

IL-19 induces production of IL-6 and TNF-alpha and results in cell apoptosis through TNF-alpha

Ist Teil von

• The Journal of immunology (1950), 2002-10, Vol.169 (8), p.4288-4297

Ort / Verlag

United States

Erscheinungsjahr

2002

Quelle

MEDLINE

Beschreibungen/Notizen

• IL-10 is an immunosuppressive cytokine in the immune system. It was in clinical trial 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.