摘要
目的探讨变应性鼻炎(AR)屋尘螨特异性免疫治疗前后外周血调节性T细胞(T regulatory cells,Treg)Foxp3基因和γδT细胞抗原识别受体(T cell receptor,TCR)Vγ亚家族基因表达的变化情况。方法选择22例屋尘螨皮下注射免疫治疗1年有效的AR患者,采用RT-PCR检测治疗前后外周血Foxp3与TCR VγⅠ~Ⅲ基因表达水平。10例健康志愿者为对照。结果 22例AR患者免疫治疗前Foxp3、TCR VγⅠ~Ⅲ水平明显低于对照组(Z=-2.155,Z=-2.114,t=4.101、t=3.108,P均〈0.05),治疗后Foxp3、VγⅢ明显升高(t=-4.577,Z=-3.416,P均〈0.05);治疗前Foxp3与VγⅠ、Ⅱ、Ⅲ呈正相关,治疗后Foxp3与VγⅢ呈正相关。结论免疫治疗1年有效的AR患者中,治疗前后外周血Treg细胞和γδT细胞亚群之间存在动态平衡关系,患者免疫治疗早期症状的改善可能与T细胞的免疫重塑相关。
OBJECTIVE To investigate the expression pattern of Treg's Foxp3 gene and γδT cell receptor(TCR) Vγ subfamily genes in peripheral blood mononuclear cells(PBMCs) of allergic rhinitis(AR) patients before and after allergen-specific immunotherapy(SIT). METHODS Twenty-two AR patients undergoing effective SIT with house dust mite extract for one year were recruited. Real-time PCR was performed to detect the gene expression levels of Foxp3 and TCR Vγ subfamilies. Ten healthy volunteers were recruited as the controls. RESULTS The expression levels of Foxp3 and TCR VγⅠ, Ⅱ, Ⅲ in AR patients before SIT were significantly lower than those in healthy subjects(Z=-2.155, P〈0.05; Z=-2.114, P〈0.05; t=4.101, P〈0.05; t=3.108, P〈0.05, respectively). The expression levels of Foxp3 and TCR VγⅢ were obviously increased after SIT(t=-4.577, P〈0.05; Z=-3.416, P〈0.05). Before SIT, significant positive correlation was observed between expression levels of Foxp3 and VγⅠ, Ⅱ, Ⅲ. After SIT, significant positive correlation was observed between expression levels of Foxp3 and VγⅢ. CONCLUSION Treg and Vγ subfamily T cells were in a dynamic balance in the PBMCs of AR patients before and after effective immunotherapy for one year. The early improvement of symptoms following immunotherapy might be associated with the remodeling of T cell immunity.
出处
《中国耳鼻咽喉头颈外科》
CSCD
2014年第9期477-480,共4页
Chinese Archives of Otolaryngology-Head and Neck Surgery
基金
国家自然科学基金(81371072)
广东省自然科学基金(S2013010016386)联合资助
关键词
变态反应和免疫学
鼻炎
变应性
常年性
抗原
尘螨属
脱敏法
免疫
T淋巴细胞
调节性
Allergy and Immunology
Rhinitis
Allergic
Perennial
Antigens
Dermatophagoides
Desensitization
Immunologic
T-Lymphocytes
Regulatory