Molecular cloning of chicken interleukin-17B, which induces proinflammatory cytokines through activation of the NF-kappa B signaling pathwayopen access
- Authors
- Hoang, Cong Thanh; Hong, Yeojin; Truong, Anh Duc; Lee, Janggeun; Lee, Kyungbaek; Hong, Yeong Ho
- Issue Date
- Sep-2017
- Publisher
- ELSEVIER SCI LTD
- Keywords
- Chicken; IL-17B; NF-KB; Signal transduction; Cytokine
- Citation
- DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY, v.74, pp 40 - 48
- Pages
- 9
- Journal Title
- DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
- Volume
- 74
- Start Page
- 40
- End Page
- 48
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/3960
- DOI
- 10.1016/j.dci.2017.04.010
- ISSN
- 0145-305X
1879-0089
- Abstract
- Interleukin (IL)-17B is a little known member of the IL -17 cytokine family, which plays an important role in immunity by regulating the expression of proinflammatory cytokines. In this study, we determined the coding sequence and biological functions of a novel chicken IL-17B (chlL-17B). The full-length chIL-17B coding sequence includes 567 nucleotides encoding 188 amino acids, which was identified in small intestinal epithelial cells. The chIL-17B protein shares 96.48% amino acid sequence identity with turkey, 92.57% with duck, and 44.92-64.06% with mammalian IL-17B proteins. ChIL-17B shares three exons and two introns with mammals, turkey, and duck. Moreover, IL-17B mRNA was more highly expressed than IL-17A mRNA in several organs of chickens infected with Salmonella and was upregulated in chicken cell lines following LPS stimulation. In addition, in chicken cell lines, chlL-17B induced the mRNA expression of several proinflammatory cytokines, including IL-1 beta, IL-6, LITAF, and INF-gamma, but not IL-17A, and activated MyD88, TAK1, NF-031, and SOCS1, which are associated with the NF-kappa B signaling pathway. Taken together, chicken interleukin-17B plays a critical role in host defense against the bacterial pathogens, and regulates proinflammatory cytokines by activating the NF-kappa B signaling pathway. (C) 2017 Elsevier Ltd. All rights reserved.
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