Chicken IL-26 regulates immune responses through the JAK/STAT and NF-kB signaling pathways

• Published in: Developmental and comparative immunology Vol. 73; p. 10
• Main Authors: Truong, Anh Duc, Hong, Yeojin, Hoang, Cong Thanh, Lee, Janggeun, Hong, Yeong Ho
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Science Ltd 01.08.2017
• Subjects: Biotechnology; Carbon tetrachloride; CCL4 protein; Cell activation; Cell lines; Cell proliferation; Chemokines; Cytokines; Gene expression; Helper cells; Immune response; Immune system; Induced polarization; Inflammation; Interleukin 10; Interleukin 12; Interleukin 4; Janus kinase 2; Lymphocytes; Lymphocytes T; Macrophages; MyD88 protein; NF-κB protein; Nitric oxide; Phosphorylation; Poultry; Regulators; Serine; Signal transduction; Signaling; Stat1 protein; Stat3 protein; Stimulation; Tyk2 protein; Tyrosine; α-Interferon; β-Interferon
• ISSN: 0145-305X; 1879-0089

Chicken interleukin 26 (ChIL-26), a member of the IL-10 family, is expressed in T cells and can induce expression of proinflammatory cytokines. We examined the response of signal transduction pathways to ChIL-26 stimulation in the chicken T(CU91), macrophage (HD11), and fibroblast (OU2) cell lines. ChIL-26 activated JAK2 and TYK2 phosphorylation, as well as activation of STAT1, STAT3, and SHP2 via tyrosine/ serine residues. We also showed that ChIL-26 activates the phosphorylation of NF-KB1, TAKI, and MyD88 kinase, which are key regulators of NF-KB signaling pathways. Moreover, ChIL-26 stimulation upregulated mRNA expression of chemokines (CCL4, CCL2O, and CXCL14), Thi (IFN-α, IFN-β, IFN-y, IL-1β, and IL- 6), Th2 (IL-4 and IL-10), and Th17 (IL-12p40, IL-17A, and IL-17F), and the Treg cytokines (TGF-(β4); additionally, it increased Th1 and Th17 protein levels and nitric oxide production but did not affect cell proliferation. Together, these results suggest that ChIL-26-induced activation of chemokines, Th1, Th2, and, Th17, and the Treg cytokines is mediated through JAK/STAT and NF-KB signaling pathways in chicken T, macrophage, and fibroblast cell lines. These results indicate a key role for ChIL-26-induced polarization of the immune response and could reveal new therapeutic approaches for use in combination with molecules that activate T and macrophage cells via activation JAK/STAT and NF-KB signaling pathways.