title: IL-17 Induces Fetal Loss in a CBA/J×BALB/c Mouse Model, and an Anti-IL-17 Antibody Prevents Fetal Loss in a CBA/J×DBA/2 Mouse Model.
abstract: OBJECTIVE
  Many researchers have demonstrated that the expression of interleukin-17(IL-17) is higher in spontaneous abortion. However, whether Th17 cells are an independent factor in inducing abortion is not known.
  
  
  METHODS
  This study investigated the effect of exogenous recombinant IL-17 and an anti-IL-17 antibody in a normal and an abortion mouse model using flow cytometry, enzyme-linked immunosorbent assay, real-time PCR, and Western blot.
  
  
  RESULTS
  Th17 cells and the related factors, IL-17 and RORγt, were significantly upregulated in abortion mice, and Treg cells and the related factor, Foxp3, were downregulated. Intraperitoneal injection of recombinant IL (rIL)-17 induced fetal loss in a normal mouse model, and an anti-IL-17 antibody prevented fetal loss in an abortion mouse model.
  
  
  CONCLUSIONS
  This study confirmed an imbalance of the Th17/Treg paradigm in abortion mice and IL-17 as a risk factor of fetal loss. An anti-IL-17 antibody may prevent abortion.
authors.affiliation: Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: Wang-Ming
authors.initials: WM
authors.lastname: Xu
authors.affiliation: Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: Zhuo-Ni
authors.initials: ZN
authors.lastname: Xiao
authors.affiliation: Center for Reproductive Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
authors.forename: Xiao-Bo
authors.initials: XB
authors.lastname: Wang
authors.affiliation: Department of Obstetrics and Gynecology, Peking University Third Hospital, Haidian District, Beijing, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Huang
mesh_terms: D000022:Abortion, Spontaneous / Q000276:immunology* / Q000517:prevention & control; D000818:Animals; D019138:Antibodies, Blocking / Q000008:administration & dosage*; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D004195:Disease Models, Animal; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D020381:Interleukin-17 / Q000008:administration & dosage*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology*; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology*
chemical_list: D019138:Antibodies, Blocking; D000911:Antibodies, Monoclonal; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3
keywords: Abortion; antibody; interleukin-17; regulatory T cells