title: Lipopolysaccharide (LPS)-induced Interferon (IFN)-gamma production by decidual mononuclear cells (DMNC) is interleukin (IL)-2 and IL-12 dependent.
abstract: OBJECTIVE
  Th1-shifted immune response is believed to be harmful for successful pregnancy because of activation of maternal cytotoxic T lymphocytes and natural killer cells. However, its effects on Toll-like receptor (TLR)-mediated innate immune response are so far unknown and this study has been undertaken to address the issue.
  
  
  METHODS
  decidual tissues were obtained from 16 pregnant women undergoing elective termination during the first trimester pregnancy for socioeconomic reasons. Decidual Mononuclear Cells (DMNC) were stimulated with suboptimal doses of IL-2 and IL-12 with/without LPS, considered to be a TLR4 ligand, for 48 hr. Productions of IFN-γ and tumor necrosis factor (TNF)-α in culture supernatant were measured with ELISA.
  
  
  RESULTS
  (i) IFN-γ production was induced with LPS alone which was strongly up-regulated in the presence of IL-2 and IL-12. (ii) TNF-α was also induced by LPS but was not affected by the presence of IL-2 and IL-12.
  
  
  CONCLUSIONS
  IL-2 and IL-12 up-regulated the production of IFN-γ in DMNC through increasing their susceptibility to LPS. TNF-α production is independent of such a mechanism.
authors.affiliation: Department of Pathology and Microbiology, Division of Microbiology, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: Masami
authors.initials: M
authors.lastname: Negishi
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Izumi
authors.forename: Sheikh
authors.initials: S
authors.lastname: Aleemuzzaman
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Inaba
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hayakawa
mesh_terms: D017252:CD3 Complex / Q000276:immunology; D019002:CD56 Antigen / Q000276:immunology; D003656:Decidua / Q000166:cytology / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D004357:Drug Synergism; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism / Q000494:pharmacology*; D007376:Interleukin-2 / Q000378:metabolism / Q000494:pharmacology*; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D017252:CD3 Complex; D019002:CD56 Antigen; D007376:Interleukin-2; D008070:Lipopolysaccharides; C522918:NCAM1 protein, human; D012333:RNA, Messenger; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D007371:Interferon-gamma