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目的:观察胸腺基质淋巴细胞生成素(TSLP)对血小板功能的影响。方法:采用血小板荧光-聚集分析仪检测TSLP刺激对血小板聚集功能及血小板ATP释放反应的影响;用流式细胞术(FCM)检测血小板表面TSLP受体(TSLPR)的表达,检测TSLP、胶原刺激和TSLP受体阻断下血小板膜蛋白的表达。结果:20位健康志愿者TSLPR-PE荧光标记阳性的血小板百分率为(7.30±3.58)%。TSLP刺激组血小板聚集及ATP释放分别为(0.6±0.8)%及(0.06±0.08)%;TSLP加胶原共刺激组血小板聚集及ATP释放明显高于胶原刺激组(P<0.01);TSLPR抗体组血小板聚集及ATP释放明显低于TSLP加胶原共刺激组(P<0.05)。TSLP刺激组及TSLP加胶原共刺激组血小板膜糖蛋白CD63、CD62p及PAC-1表达与对照组相比均增加(均P<0.05)。TSLP加胶原共刺激组与对照组相比CD42b表达明显下降(P<0.01);TSLP加胶原刺激组与胶原刺激组相比,CD62、CD63、PAC-1表达明显上升,CD42b的表达明显下降(均P<0.05);TSLPR抗体组与TSLP加胶原刺激组相比,CD62、CD63、PAC-1表达明显下降(均P<0.05),CD42b的表达变化不明显。结论:正常人血小板表面存在TSLPR。TSLP可增强胶原诱导血小板聚集及释放,并可通过TSLPR促进血小板活化。
Objective: To observe the effect of thymic stromal lymphopoietin (TSLP) on platelet function. Methods: The effect of TSLP stimulation on platelet aggregation and platelet ATP release was tested by platelet fluorescence-aggregation analyzer. The expression of TSLP receptor on TSLP was detected by flow cytometry (FCM) TSLP receptor blockade of platelet membrane protein expression. Results: The percentage of TSLPR-PE positive fluorescent platelets in 20 healthy volunteers was (7.30 ± 3.58)%. TSLP stimulated platelet aggregation and ATP release were (0.6 ± 0.8)% and (0.06 ± 0.08)%, respectively. TSLP plus collagen co-stimulated platelet aggregation and ATP release were significantly higher than those in collagen-stimulated group (P <0.01) Platelet aggregation and ATP release were significantly lower than TSLP plus collagen co-stimulation group (P <0.05). TSLP stimulation group and TSLP plus collagen co-stimulation group platelet membrane glycoprotein CD63, CD62p and PAC-1 expression compared with the control group were increased (P <0.05). The expression of CD42b in TSLP plus collagen costimulation group was significantly lower than that in control group (P <0.01). Compared with collagen stimulation group, the expressions of CD42b, CD63 and PAC-1 in TSLP plus collagen stimulation group were significantly increased and the expression of CD42b was significantly decreased (P <0.05). Compared with TSLP plus collagen stimulation group, the expressions of CD62, CD63 and PAC-1 in TSLPR antibody group were significantly decreased (all P <0.05), while the expression of CD42b did not change significantly. Conclusion: TSLPR exists on the surface of normal human platelets. TSLP can enhance collagen-induced platelet aggregation and release, and can promote platelet activation by TSLPR.