摘要
目的Ⅱ型固有淋巴细胞(group Ⅱ innate lymphoid cells,ILC2)是近年来新发现的非T非B淋巴细胞,在IL-25或IL-33刺激下产生和分泌IL-5、IL-13等2型免疫应答的细胞因子,参与Th2优势分化状态的维持。桥本甲状腺炎(Hashimoto’s thyroiditis,HT)是一类器官特异性的自身免疫性疾病,其甲状腺球蛋白抗体(ATG)和甲状腺过氧化物酶抗体(ATPO)等自身抗体均显著升高。ILC2参与的Th2细胞应答是介导抗体产生的重要途径,其与HT自身抗体的产生关系尚未见报道。方法本研究采用q RT-PCR法检测HT患者外周血ILC2特征性细胞因子和转录因子的表达水平,并对其与血清ATG和ATPO水平的相关性进行了分析。结果 HT患者外周血单个核细胞(PBMC)ILC2特征性转录因子(RORα)和细胞因子(IL-13)的m RNA明显增加,且与血清ATG及ATPO自身抗体水平的显著升高呈现明显正相关。结论 ILC2的活性与HT患者自身抗体的产生有着密切的关系,其作用可能是通过维持Th2极化状态促进自身抗体的产生,拟或影响IL-10的产生降低自身抗体应答的负向调控,有待进一步深入研究。
Group Ⅱ innate lymphoid cells(ILC2) is a newly discovered non B non T lymphocyte, which iscapable of producing large amounts of IL-13 and IL-5 when stimulated by IL-25 and IL-33, and participate in themaintenance of Th2 cell polarization. Hashimoto's thyroiditis is a kind of organ specific autoimmune diseaseaccompanied by increased levels of autoantibodies such as ATG and ATPO in serum of patients. The relationshipbetween ILC2 and autoantibodies has not been reported in Hashimoto's thyroiditis. In this study, we detected theexpression levels of ILC2-associated cytokines and transcription factor in peripheral blood from patients withHashimoto's thyroiditis, and analyzed the correlation between the expression levels of ILC2-associated cytokinesand autoantibodies. The results showed that the expression levels of ILC2-associated cytokines and transcriptionfactor were significantly increased in Hashimoto's thyroiditis, and the increased level of ILC2-associated moleculeswere positively or modestly correlated with ATG or ATPO autoantibody. All result prompted that the activity of ILC2 is closely related to autoantibodies production in patients with Hashimoto thyroiditis, which may be performed bymaintaining the Th2 polarization or inhibiting IL-10 secretion.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2017年第4期338-342,共5页
Immunological Journal
基金
国家自然科学基金(31270947)
江苏省重点研发计划(BE2016716)
江苏省高校自然科学研究重大项目(16KJA320005)
关键词
桥本甲状腺炎
Ⅱ型固有淋巴细胞
自身抗体
转录因子
细胞因子
Hashimoto's thyroiditis
Group Ⅱ innate lymphoid cells
Autoantibodies
Transcription factor
Cytokine