title: The SWI/SNF chromatin-remodeling complex modulates peripheral T cell activation and proliferation by controlling AP-1 expression.
abstract: The SWI/SNF chromatin-remodeling complex has been implicated in the activation and proliferation of T cells. After T cell receptor signaling, the SWI/SNF complex rapidly associates with chromatin and controls gene expression in T cells. However, the process by which the SWI/SNF complex regulates peripheral T cell activation has not been elucidated. In this study, we show that the SWI/SNF complex regulates cytokine production and proliferation of T cells. During T cell activation, the SWI/SNF complex is recruited to the promoter of the transcription factor AP-1, and it increases the expression of AP-1. Increased expression of the SWI/SNF complex resulted in enhanced AP-1 activity, cytokine production, and proliferation of peripheral T cells, whereas knockdown of the SWI/SNF complex expression impaired the AP-1 expression and reduced the activation and proliferation of T cells. Moreover, mice that constitutively expressed the SWI/SNF complex in T cells were much more susceptible to experimentally induced autoimmune encephalomyelitis than the normal mice were. These results suggest that the SWI/SNF complex plays a critical role during T cell activation and subsequent immune responses.
authors.affiliation: Department of Biological Sciences, Institute of Molecular Biology and Genetics, and Research Center for Functional Cellulomics, Seoul National University, 599 Gwanangno, Gwanak-gu, Seoul 151-742, Korea.
authors.forename: Seung Min
authors.initials: SM
authors.lastname: Jeong
authors.forename: Changjin
authors.initials: C
authors.lastname: Lee
authors.forename: Sung Kyu
authors.initials: SK
authors.lastname: Lee
authors.forename: Jieun
authors.initials: J
authors.lastname: Kim
authors.forename: Rho Hyun
authors.initials: RH
authors.lastname: Seong
mesh_terms: D000818:Animals; D018801:CD2 Antigens / Q000235:genetics / Q000378:metabolism; D002455:Cell Division / Q000276:immunology; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000503:physiopathology*; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D016762:Genes, fos / Q000502:physiology; D016758:Genes, jun / Q000502:physiology; D008213:Lymphocyte Activation / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D011401:Promoter Regions, Genetic / Q000502:physiology; D013601:T-Lymphocytes / Q000166:cytology / Q000502:physiology*; D018808:Transcription Factor AP-1 / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics / Q000276:immunology* / Q000378:metabolism
chemical_list: D018801:CD2 Antigens; D016207:Cytokines; C491090:Smarcc1 protein, mouse; D018808:Transcription Factor AP-1; D014157:Transcription Factors