HMGB1和TLR9在系统性红斑狼疮发病机制中的作用

Study on Effect of HMGB1 and TLR9 in the Pathogenesis of Systemic Lupus Erythematosus

目的探讨高迁移率族蛋白1(HMGB1)和Toll样受体9(TLR9)在SLE发病中的作用。方法随机选取活动期与缓解期SLE患者各40例,健康对照组40例,采用酶联免疫吸附试验(ELISA)法检测血清中HMGB1蛋白的表达,采用流式细胞技术(FCM)检测外周血单核细胞上TLR9的表达。分析HMGB1,TLR9与SLE病情活动的相关性。结果 SLE活动期组血清HMGB1表达水平较缓解期组和健康对照组明显增高(P<0.05),而SLE缓解期组和健康对照组血清HMGB1表达水平差异无统计学意义(P>0.05);活动期组SLE患者外周血单核细胞TLR9的表达较缓解期组和健康对照组相比呈上调趋势,而TLR9的表达在SLE缓解期组和健康对照组之间差异无统计学意义;血清中HMGB1的表达水平与外周血单核细胞表面TLR9的表达呈正相关。结论血清HMGB1和外周血单核细胞表面TLR9均参与了SLE的病情发展过程,且其在SLE发病机制中可能具有协同作用。

Objective To explore the effect of high mobility group proteinl （ HMGBI ） and Toll-like receptor-9 （TLR9） in the pathogenesis of systemic lupus erythematosus （ SLE ）. Methods Forty patients with SLE of active phase and 40 patients with SLE of paracmasis were selected randomly, and 40 volunteers with healthy body were acted as control groups. Enzyme linked immunosorbent assay（ELISA） was used to test the expression of serum HMGB1 protein and flow cytometry（FCM） was used to test the expression of TLR9 in the peripheral blood monouclear cells （PBMC）. The correlation between HMGB1, TLR9 and the patient＇s condition of SLE was analyzed. Results The expressing level of serum HMGB1 was more high in SLE of active phase groups than that in SLE of paracmasis groups and control groups （ P 〈 0.05 ）, but there was no significant differences in the expression of serum HMGB1 between the paracmasis groups and control groups（P 〉0.05）.The expressing level of TLR9 on the peripheral blood monouclear cells was more high in the SLE of active phase groups than the SLE of paracmasis groups and control groups（P 〈0.05） , but there was no significant difference in the expressing pattern between the SLE paracmasis groups and the control groups. It showed positive correlation in the expressing level of serum HMGB1 and TLR9 in the peripheral blood monouclear cells. Conclusion The serum HMGB1 and TLR9 on the peripheral blood monouclear cells all participated in the process of development in SLE and played synergistic effect during the pathogenesis of SLE.