IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells

IntroductionSchistosomiasis japonica, a zoonotic parasitic disease, induces complex immune regulation during infection. The inflammatory responses and immunosuppressive mechanisms co-exist to maintain immune homeostasis in schistosomiasis. B7-H4 is a critical immune checkpoint molecule that modulate...

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Main Authors: Dandan Zhu, Guo Chen, Pei Shen, Weiliang Fan, Chuxin Ji, Yinong Duan, Wenxi Gao
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-08-01
Series:Frontiers in Cellular and Infection Microbiology
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Online Access:https://www.frontiersin.org/articles/10.3389/fcimb.2025.1613297/full
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author Dandan Zhu
Guo Chen
Guo Chen
Pei Shen
Weiliang Fan
Chuxin Ji
Yinong Duan
Wenxi Gao
Wenxi Gao
author_facet Dandan Zhu
Guo Chen
Guo Chen
Pei Shen
Weiliang Fan
Chuxin Ji
Yinong Duan
Wenxi Gao
Wenxi Gao
author_sort Dandan Zhu
collection DOAJ
description IntroductionSchistosomiasis japonica, a zoonotic parasitic disease, induces complex immune regulation during infection. The inflammatory responses and immunosuppressive mechanisms co-exist to maintain immune homeostasis in schistosomiasis. B7-H4 is a critical immune checkpoint molecule that modulates T cell activation and exerts immunosuppressive effects. Our previous investigations revealed that B7-H4 mRNA expression was elevated in mice infected with Schistosoma japonicum, with interleukin-10 (IL-10) demonstrating regulatory capacity to enhance B7-H4 expression in RAW264.7 macrophages. In this study, we further explore the mechanism underlying IL-10-mediated B7-H4 upregulation.MethodsWestern blot was performed to detect B7-H4 expression levels, both in mice infected with Schistosoma japonicum and in RAW264.7 cells stimulated with IL-10. RT-qPCR was performed to screen microRNAs (miR-140 et al.) in RAW264.7 cells stimulated with IL-10. Then dual-luciferase reporter assay was performed to confirm that miR-140 can directly bind to the 3’UTR of B7-H4. miR-140 promoter activity in RAW264.7 cells was also detected via dual-luciferase reporter assays. In addition, ChIP was performed to confirm the binding of transcription factors and miR-140 promoter.ResultsNotably, miR-140 was decreased in IL-10-treated microphages, accompanied by B7-H4 expression was upregulated. miR-140 can directly bind to the 3’UTR of B7-H4 and then inhibit the expression of B7-H4 in RAW264.7 cells. Meanwhile, miR-140 mimics can also attenuate IL-10-induced B7-H4 expression in RAW264.7 cells. Then we found that IL-10 may inhibit miR-140 promoter activity in RAW264.7 cells through transcription factors that binding to the - 576/- 94 bp region of the miR-140 promoter. Results by Western blot and ChIP further indicated that IL-10 could downregulate miR-140 promoter activity in a STAT5 dependence manner. After the sequence of STAT5 binding site within the - 456/- 446 bp region of the miR-140 promoter was mutated, IL-10 failed to suppress the activity produced by mutant miR-140 promoter.DiscussionIn summary, IL-10 can inhibit miR-140 through STAT5, thereby upregulating the expression of B7-H4 in RAW264.7 cells. This study may suggest a new mechanism underlying IL-10-mediated B7-H4 upregulation in macrophages.
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spelling doaj-art-001bab3ce2ec463bb9beea026c6c6f412025-08-20T03:05:53ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882025-08-011510.3389/fcimb.2025.16132971613297IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cellsDandan Zhu0Guo Chen1Guo Chen2Pei Shen3Weiliang Fan4Chuxin Ji5Yinong Duan6Wenxi Gao7Wenxi Gao8Department of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, ChinaDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, ChinaDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu, ChinaLaboratory Center, School of Educational Sciences, Nantong University, Nantong, Jiangsu, ChinaIntroductionSchistosomiasis japonica, a zoonotic parasitic disease, induces complex immune regulation during infection. The inflammatory responses and immunosuppressive mechanisms co-exist to maintain immune homeostasis in schistosomiasis. B7-H4 is a critical immune checkpoint molecule that modulates T cell activation and exerts immunosuppressive effects. Our previous investigations revealed that B7-H4 mRNA expression was elevated in mice infected with Schistosoma japonicum, with interleukin-10 (IL-10) demonstrating regulatory capacity to enhance B7-H4 expression in RAW264.7 macrophages. In this study, we further explore the mechanism underlying IL-10-mediated B7-H4 upregulation.MethodsWestern blot was performed to detect B7-H4 expression levels, both in mice infected with Schistosoma japonicum and in RAW264.7 cells stimulated with IL-10. RT-qPCR was performed to screen microRNAs (miR-140 et al.) in RAW264.7 cells stimulated with IL-10. Then dual-luciferase reporter assay was performed to confirm that miR-140 can directly bind to the 3’UTR of B7-H4. miR-140 promoter activity in RAW264.7 cells was also detected via dual-luciferase reporter assays. In addition, ChIP was performed to confirm the binding of transcription factors and miR-140 promoter.ResultsNotably, miR-140 was decreased in IL-10-treated microphages, accompanied by B7-H4 expression was upregulated. miR-140 can directly bind to the 3’UTR of B7-H4 and then inhibit the expression of B7-H4 in RAW264.7 cells. Meanwhile, miR-140 mimics can also attenuate IL-10-induced B7-H4 expression in RAW264.7 cells. Then we found that IL-10 may inhibit miR-140 promoter activity in RAW264.7 cells through transcription factors that binding to the - 576/- 94 bp region of the miR-140 promoter. Results by Western blot and ChIP further indicated that IL-10 could downregulate miR-140 promoter activity in a STAT5 dependence manner. After the sequence of STAT5 binding site within the - 456/- 446 bp region of the miR-140 promoter was mutated, IL-10 failed to suppress the activity produced by mutant miR-140 promoter.DiscussionIn summary, IL-10 can inhibit miR-140 through STAT5, thereby upregulating the expression of B7-H4 in RAW264.7 cells. This study may suggest a new mechanism underlying IL-10-mediated B7-H4 upregulation in macrophages.https://www.frontiersin.org/articles/10.3389/fcimb.2025.1613297/fullmiR-140B7-H4IL-10STAT5Schistosoma japonicum
spellingShingle Dandan Zhu
Guo Chen
Guo Chen
Pei Shen
Weiliang Fan
Chuxin Ji
Yinong Duan
Wenxi Gao
Wenxi Gao
IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
Frontiers in Cellular and Infection Microbiology
miR-140
B7-H4
IL-10
STAT5
Schistosoma japonicum
title IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
title_full IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
title_fullStr IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
title_full_unstemmed IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
title_short IL-10/STAT5 axis suppresses miR-140 to upregulate B7-H4 expression in RAW264.7 cells
title_sort il 10 stat5 axis suppresses mir 140 to upregulate b7 h4 expression in raw264 7 cells
topic miR-140
B7-H4
IL-10
STAT5
Schistosoma japonicum
url https://www.frontiersin.org/articles/10.3389/fcimb.2025.1613297/full
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