title: STAT4 is required for IFN-β-induced MCP-1 mRNA expression in murine mast cells.
abstract: BACKGROUND
  Mast cells are immunocompetent cells that are found in almost all tissues and function as sentinels of immune responses. Recently, it has been shown that mast cells play significant roles in innate immune responses. However, it is still largely unknown whether signal transducers and activators of transcription 4 (STAT4), one of the STAT proteins under type I IFN signaling, is involved in type I IFN-mediated gene expression in mast cells.
  
  
  METHODS
  We investigated the role of STAT4 in IFN-β-induced gene expression in mast cells by using STAT4-deficient (STAT4(-/-)) bone marrow-derived mast cells (BMMCs).
  
  
  RESULTS
  STAT4 was expressed in BMMCs and activated in response to IFN-β but not to IL-12 or IL-23. The development of BMMCs as well as IgE-induced degranulation of BMMCs was normal in STAT4(-/-) mice. On the other hand, while IFN-β-induced mRNA expression of interferon-induced protein with tetratricopeptide repeats 1 (IFIT-1), protein kinase interferon-inducible double stranded RNA dependent (PKR), and myxovirus resistance 1 (Mx1) was similar between STAT4(-/-) BMMCs and wild-type (WT) BMMCs, IFN-β-induced MCP-1 mRNA expression was severely diminished in STAT4(-/-) BMMCs as compared with WT BMMCs.
  
  
  CONCLUSIONS
  STAT4 plays an essential role in IFN-β-induced MCP-1 mRNA expression in mast cells.
authors.affiliation: Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Kazuma
authors.initials: K
authors.lastname: Iida
authors.forename: Kotaro
authors.initials: K
authors.lastname: Suzuki
authors.forename: Masaya
authors.initials: M
authors.lastname: Yokota
authors.forename: Daiki
authors.initials: D
authors.lastname: Nakagomi
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Wakashin
authors.forename: Arifumi
authors.initials: A
authors.lastname: Iwata
authors.forename: Hirotoshi
authors.initials: H
authors.lastname: Kawashima
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Takatori
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakajima
mesh_terms: D000818:Animals; D015550:Cell Degranulation / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D018932:Chemokine CCL2 / Q000235:genetics*; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation / Q000276:immunology*; D016899:Interferon-beta / Q000494:pharmacology*; D007377:Interleukin-3 / Q000494:pharmacology; D008407:Mast Cells / Q000166:cytology / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010766:Phosphorylation / Q000187:drug effects; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D017455:Receptors, IgE / Q000819:agonists / Q000378:metabolism; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050797:STAT4 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D001619:beta-N-Acetylhexosaminidases / Q000378:metabolism
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D007377:Interleukin-3; D017455:Receptors, IgE; D050794:STAT1 Transcription Factor; D050797:STAT4 Transcription Factor; C494080:Stat1 protein, mouse; C494091:Stat4 protein, mouse; D016899:Interferon-beta; D019009:Proto-Oncogene Proteins c-kit; D001619:beta-N-Acetylhexosaminidases