Objective: To investigate the roles of the chemokine receptor CXCR3 and its ligand I-TAC in the pathogenesis of immune thrombocytopenic purpura (ITP).
Methods: A total of 48 ITP patients were enrolled in this study: 30 with newly diagnosed or relapse ITP and 18 in remission after treatment, and 24 healthy volunteers were as controls. IFNγ and I-TAC in plasma were detected by ELISA. The mRNA expression of CXCR3 in the peripheral blood mononuclear cells (PBMNCs) was determined by quantitative RT-PCR.
Results: The IFNγ level in the plasma of ITP patients before the treatment was obviously increased than those in the remission group and controls [(71.45 ± 17.62) ng/L vs (36.94 ± 14.86) ng/L and (25.28 ± 12.85) ng/L, all P < 0.05] and those in the remission group was higher than in the controls (P < 0.05). In contrast, there were no statistic differences of the levels of I-TAC among the three groups [(455.56 ± 144.70) ng/L, (488.24 ± 164.70) ng/L and (382.97 ± 167.43) ng/L, P > 0.05]. Both ITP patients before the treatment and remission groups expressed more CXCR3 mRNA [6.76 (3.03, 37.00), 1.76 (0.45, 14.18) vs 0.12 (0.04, 0.28), P < 0.05]. After effective therapy, CXCR3 mRNA expression decreased, while it was still higher than that in the controls.
Conclusions: Our data demonstrate that Th1 cytokine (IFNγ) dominance is reflected in ITP. Simultaneously, the CXCR3(+) cell may play a role in cell-mediated immunity through chemotaxis in ITP.