Relationship between expression of chemokine receptors CCR3,CCR5 and CXCR3 on CD4+ T cells and spont

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Background Previous studies have shown that local immune cells in the feto-matal interface are recruited from peripheral blood, and that chemokines and their receptors play an initial and key role in this recruitment process. In this study, we aimed to determine whether spontaneous abortion is associated with the expression of chemokine receptors CCR3, CCR5, and CXCR3 on CD4+ T cells.Methods Peripheral blood, spleen, and thymus were collected from the spontaneous abortion mouse model CBA/J×DBN2 (SA group, n=14), the normal pregnant mouse model CBA/J×BALB/c (NP group, n=13), and normal non-pregnant CBA/J mice (NNP group, n=11). The number of chemokine receptors CCR3, CCR5, and CXCR3 expressed on CD4+ T cells was measured by double-label flow cytometry (FCM) method.Results In peripheral blood, the SA group had significantly lower CCR3 expression (P <0.01) and higher CCR5 and CXCR3 expression (P <0.01) on CD4+ T cells than did the NP group. But comparing these chemokines between the SA and NNP groups, there was no significant difference (P >0.05). In spleen, the SA group expressed significantly lower CCR3 expression (P <0.01) and higher CCR5 and CXCR3 expression (P <0.05) on CD4+ T cells than did the NP group. When compared with the NNP group, the SA group had significantly higher CCR3 expression (P <0.01), but was not statistically different with regards to the other two chemokines (P >0.05). In thymus, the SA group had significantly lower CCR3 expression (P <0.05) and higher CXCR3 expression (P <0.05) on CD4+ T cells than the NP group, with no significant difference in CCR5 expression (P >0.05). Compared with the NNP group, the SA group had higher CCR3 expression (P <0.01), but there was no statistical difference in CXCR3 and CCR5 expression (P >0.05) between the two groups.Conclusion The abnormal expression of CCR3, CCR5 and CXCR3 on CD4+ T cells may play an important role in the pathogenesis of spontaneous abortion.
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