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

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

Research output: Contribution to journalArticlepeer-review

166 Citations (Scopus)

Abstract

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-α. 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-α and induces apoptosis.

Original languageEnglish
Pages (from-to)4288-4297
Number of pages10
JournalJournal of Immunology
Volume169
Issue number8
DOIs
Publication statusPublished - 2002 Oct 15

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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