title: MicroRNA-155 modulates Treg and Th17 cells differentiation and Th17 cell function by targeting SOCS1.
abstract: MicroRNA (miR)-155 is a critical player in both innate and adaptive immune responses. It can influence CD4(+) T cell lineage choice. To clarify the role of miR-155 in CD4(+) CD25(+) regulatory T (Treg)/T helper (Th)17 cell differentiation and function, as well as the mechanism involved, we performed gain-and loss-of-function analysis by transfection pre-miR-155 and anti-miR-155 into purified CD4(+) T cells. The results showed that miR-155 positively regulated both Treg and Th17 cell differentiation. It also induced the release of interleukin (IL)-17A by Th17 cells, but not the release of IL-10 and transforming growth factor (TGF)-β1 by Treg cells. Furthermore, we found that miR-155 reacted through regulating Janus kinase/signal transducer and activator of transcription (JAK/STAT) rather than TGF-β/mothers against decapentaplegic homolog (SMAD) signaling pathway in the process of Treg and Th17 cells differentiation. This may because suppressors of cytokine signaling (SOCS)1, the important negative regulator of JAK/STAT signaling pathway, was the direct target of miR-155 in this process, but SMAD2 and SMAD5 were not. Therefore, we demonstrated that miR-155 enhanced Treg and Th17 cells differentiation and IL-17A production by targeting SOCS1.
authors.affiliation: Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Yao
authors.forename: Yu-Lan
authors.initials: YL
authors.lastname: Ma
authors.forename: Wei
authors.initials: W
authors.lastname: Liang
authors.forename: Huan-Huan
authors.initials: HH
authors.lastname: Li
authors.forename: Zhi-Jun
authors.initials: ZJ
authors.lastname: Ma
authors.forename: Xian
authors.initials: X
authors.lastname: Yu
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
mesh_terms: D000818:Animals; D001483:Base Sequence; D002454:Cell Differentiation / Q000235:genetics*; D051858:Forkhead Transcription Factors / Q000235:genetics; D050990:GATA3 Transcription Factor / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism; D053612:Janus Kinases / Q000378:metabolism; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D050791:STAT Transcription Factors / Q000378:metabolism; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics*; D020825:T-Box Domain Proteins / Q000235:genetics / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000166:cytology* / Q000378:metabolism*; D058504:Th17 Cells / Q000166:cytology* / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D000098815:T-bet Transcription Factor
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D050990:GATA3 Transcription Factor; D020381:Interleukin-17; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D050791:STAT Transcription Factors; D051785:Smad Proteins; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D053773:Transforming Growth Factor beta1; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma; D053612:Janus Kinases