TY - JOUR
T1 - Characterization of orange-spotted grouper (Epinephelus coioides) interferon regulatory factor 4 regulated by heat shock factor 1 during heat stress in response to antiviral immunity
AU - Lai, Chai Foong
AU - Wang, Ting Yu
AU - Yeh, Min I.
AU - Chen, Tzong Yueh
N1 - Funding Information:
This research was supported by the Ministry of Science and Technology, Taiwan (MOST 103-2313-B-006-004-MY3, 105-2321-B-006-027 and 106-2321-B-006-015 ) and the Headquarters of University Advancement at the National Cheng Kung University granted by the Ministry of Education, Taiwan .
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/11
Y1 - 2020/11
N2 - Interferon regulatory factor 4 (IRF4), in conjunction with thermogenic regulation, is a negative regulator of immune responses. Therefore, we examined whether temperature changes regulated the antiviral response of IRF4 in nervous necrosis virus (NNV)-infected orange-spotted groupers. We found that osgIRF4 mRNA expression was responsive to poly I:C stimulation and NNV infection. In vitro overexpression of osgIRF4 caused a marked decrease in the promoter activity of the antiviral protein Mx1, and magnified NNV replication. Notably, we showed that the IAD domain of osgIRF4 exerted a dominant inhibitory effect on the Mx1 promoter. Furthermore, on exposure to high temperatures, the action of osgIRF4 was dependent on heat shock factor 1 (HSF1) expression. Additionally, small interfering RNA knockdown of HSF1 abrogated high temperature-mediated osgIRF4 activity. These findings suggest that osgIRF4 is an essential negative regulator of innate antiviral immunity and enhances viral replication during heat stress in the orange-spotted grouper.
AB - Interferon regulatory factor 4 (IRF4), in conjunction with thermogenic regulation, is a negative regulator of immune responses. Therefore, we examined whether temperature changes regulated the antiviral response of IRF4 in nervous necrosis virus (NNV)-infected orange-spotted groupers. We found that osgIRF4 mRNA expression was responsive to poly I:C stimulation and NNV infection. In vitro overexpression of osgIRF4 caused a marked decrease in the promoter activity of the antiviral protein Mx1, and magnified NNV replication. Notably, we showed that the IAD domain of osgIRF4 exerted a dominant inhibitory effect on the Mx1 promoter. Furthermore, on exposure to high temperatures, the action of osgIRF4 was dependent on heat shock factor 1 (HSF1) expression. Additionally, small interfering RNA knockdown of HSF1 abrogated high temperature-mediated osgIRF4 activity. These findings suggest that osgIRF4 is an essential negative regulator of innate antiviral immunity and enhances viral replication during heat stress in the orange-spotted grouper.
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U2 - 10.1016/j.fsi.2020.08.033
DO - 10.1016/j.fsi.2020.08.033
M3 - Article
C2 - 32858187
AN - SCOPUS:85090189090
SN - 1050-4648
VL - 106
SP - 755
EP - 767
JO - Fish and Shellfish Immunology
JF - Fish and Shellfish Immunology
ER -