title: [Effect of β2GPI immunization on mouse T helper cell subset differentiation].
abstract: OBJECTIVE
  To explore the mechanism of beta2 glycoprotein I (β2GPI)-caused T helper cell subset differentiation and anti-β2GPI antibody (aβ2GPI Ab) production in mice.
  
  
  METHODS
  The healthy BALB/c mice were randomly divided into two groups: normal saline (NS) group and β2GPI group. The mice were immunized i.v. with either human β2GPI or equal amount of NS for a total of two or four times at 2-week intervals. The titer of aβ2GPI Ab in mice serum was evaluated by indirect ELISA. The expressions of GATA binding protein 3 (GATA3), interleukin 4 (IL-4), T-box expressed in T cells (T-bet), interferon-γ (IFN-γ) and Foxp3 mRNAs in mouse splenic cells were detected by real-time quantitative PCR (qRT-PCR), and the percentage of GATA3+ or Foxp3+ cells in lymphocytes of mouse spleen was detected by flow cytometry.
  
  
  RESULTS
  The high titer (1:100,000) of aβ2GPI Ab was detected in mouse serum following the two times of immunization with β2GPI. The expressions of Th2 specific markers GATA3 and IL-4 mRNAs and the percentage of GATA3+ cells in lymphocytes were higher than those of NS treated group. After four times of immunization with β2GPI, the titer of aβ2GPI Ab in mouse serum was elevated to a higher level (>1:100,000). The expressions of GATA3, Th1 specific markers T-bet and IFN-γ, and regulatory T cell (Treg) specific marker Foxp3 mRNAs in mouse spleen cells, but no significant change was found in IL-4 mRNA expression. Furthermore, the percentage of GATA3+ cells in mouse spleen increased, while the percentage of Foxp3+ cells decreased.
  
  
  CONCLUSIONS
  β2GPI immunization could induce Th2 cell bias polarization and Th1 cell and Treg suppression in mice, which might contribute to the production of aβ2GPI Ab.
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Chao
authors.initials: C
authors.lastname: He
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhou
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Hongxiang
authors.initials: H
authors.lastname: Xie
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Yachao
authors.initials: Y
authors.lastname: Xie
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Xiangmin
authors.initials: X
authors.lastname: Kong
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Si
authors.initials: S
authors.lastname: Cheng
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Yinjing
authors.initials: Y
authors.lastname: Yu
authors.affiliation: School of Medicine, Jiangsu University, Zhenjiang 212013, China.
authors.forename: Longfei
authors.initials: L
authors.lastname: Xia
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007114:Immunization; D051379:Mice; D008807:Mice, Inbred BALB C; D013154:Spleen / Q000276:immunology / Q000378:metabolism; D018417:Th1 Cells / Q000166:cytology* / Q000276:immunology*; D018418:Th2 Cells / Q000166:cytology* / Q000276:immunology*; D013997:Time Factors; D053482:beta 2-Glycoprotein I / Q000276:immunology*
chemical_list: D053482:beta 2-Glycoprotein I