[Effect of β2GPI immunization on mouse T helper cell subset differentiation]

To explore the mechanism of beta2 glycoprotein I (β2GPI)-caused T helper cell subset differentiation and anti-β2GPI antibody (aβ2GPI Ab) production in mice.

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.

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.

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.