摘要
目的 探讨肿瘤坏死因子(tumor necrosis factor-α,TNF-α)及可溶性白介素2受体(solubleinterleukln-2 receptor,sIL-2R)在急性 Guillain-Barre综合征(Guillain-Barre syndrome,GBS)免疫发病机制中的作用。方法 采用双抗体夹心 ELISA法,对30例急性GBS患者外周血TNF-α及sIL-2R水平进行检测,并与24例其他神经系统疾病患者及正常对照组进行比较。结果 急性CBS患者外周血TNF-α及SIL-2R水平明显升高,与正常对照组及其他神经系统疾病组比较差异有显著性意义(P<0.01);且外周血TNF-α水平的明显增高与GBS的病情进展有关。结论 急性GBS患者有多种细胞因子异常,TNF-α、SIL-2R可能参与了急性GBS的免疫发病机制过程。
Objective To study the immunopathogenesis of tumor necrosis factor-a (TNF-a) and soluble interleukin-2 receptor (sIL-2R) in acute Guillain-Barre syndrome (GBS). Methods The levels of TNF-a and sIL-2R of peripheral blood in 30 patients with acute GBS were measured by biantibody sandwich ELISA and were compared with that in 24 patients with other neurological diseases (OND) and normal control group. Results The levels of TNF-a and sIL-2R of peripheral blood in the acute GBS patients were significantly higher than that in normal control group or OND group (P<0.01). The level of TNF-a was obviously increased and correlated directly with the severity of the diseases in acute GBS patients. Conclusion It is demonstrated that there are abnormal cytokines in acute GBS patients, and TNF-a and sIL-2R may be involved in its immunopathogenesis.
