title: miR-155 contributes to Df1-induced asthma by increasing the proliferative response of Th cells via CTLA-4 downregulation.
abstract: Allergen-induced airway inflammation is characterized by Th2-mediated eosinophilic inflammation in the lungs. While the molecular mechanisms leading to this abnormal Th2 response remain unclear. Recent studies have demonstrated that MicroRNAs (miRNAs) modulate allergic airway inflammation. In this study, the role of miRNAs in allergic asthma pathogenesis was examined. Differentially expressed miRNAs were identified via miRNA microarray, with miR-155 being among the most highly expressed in asthma mice lungs. Examination of miR-155 overexpression resulted in enhanced inflammation and mucus hypersecretion in the lungs of allergen-challenged mice compared with control animals. Furthermore, CTLA-4, an important negative regulator of T-cell activation, was identified as a direct miR-155 target. Moreover, miR-155 overexpression in CD4+T cells resulted in decreased CTLA-4 levels and a subsequent increased proliferative response. Collectively, these findings suggest that miR-155 might contribute to allergic asthma by increasing the proliferative response of Th cells via CTLA-4 downregulation and thus may be a potential therapeutic target for allergic asthma.
authors.affiliation: Laboratory Medicine of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: ying-micky@163.com.
authors.forename: Yingying
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Medical Parasitology, Wannan Medical College, Wuhu 241002, PR China. Electronic address: asdentao@126.com.
authors.forename: Entao
authors.initials: E
authors.lastname: Sun
authors.affiliation: Central Laboratory of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: lixueqin0727@163.com.
authors.forename: Xueqin
authors.initials: X
authors.lastname: Li
authors.affiliation: Central Laboratory of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: zhangmengying1983@21cn.com.
authors.forename: Mengying
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Central Laboratory of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: tangzongsheng@163.com.
authors.forename: Zongsheng
authors.initials: Z
authors.lastname: Tang
authors.affiliation: Central Laboratory of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: 921236441@qq.com.
authors.forename: Ling
authors.initials: L
authors.lastname: He
authors.affiliation: Central Laboratory of Yijishan Hospital, Wannan Medical College, Wuhu 241001, PR China. Electronic address: lvkun315@126.com.
authors.forename: Kun
authors.initials: K
authors.lastname: Lv
mesh_terms: D000818:Animals; D039741:Antigens, Dermatophagoides / Q000276:immunology; D001249:Asthma / Q000235:genetics / Q000276:immunology*; D060908:CTLA-4 Antigen / Q000235:genetics / Q000378:metabolism*; D049109:Cell Proliferation / Q000235:genetics; D002478:Cells, Cultured; D040001:Dermatophagoides farinae; D015536:Down-Regulation; D008168:Lung / Q000473:pathology*; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D035683:MicroRNAs / Q000235:genetics*; D018418:Th2 Cells / Q000502:physiology*
chemical_list: D039741:Antigens, Dermatophagoides; D060908:CTLA-4 Antigen; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse
keywords: Asthma; CTLA-4; miR-155