CAJ | 학술논문

目的观察碘过量和甲状腺球蛋白(Tg)免疫诱发甲状腺炎的病变特点,进一步了解碘过量在自身免疫性甲状腺炎发病中的作用机制.方法选用NOD小鼠,饮0.05%碘化钠(NaI)水和(或)Tg皮下免疫.观察甲状腺形态学改变和细胞凋亡情况;检测血清中TT4、TSH、甲状腺球蛋白抗体(TgAb)和甲状腺过氧化物酶抗体(TPOAb)水平;检测颈部淋巴结和脾脏淋巴细胞对Tg刺激的增殖反应和脾脏细胞培养上清中白细胞介素4(IL-4)和1γ-干扰素(IFN-γ)水平;实时荧光定量PCR法检测甲状腺绀织内IL-4、IFN-γ、趋化冈子配体10(CXCL10)、细胞间黏附因子1(ICAM-1)mRNA的表达.结果碘过量组甲状腺滤泡扩张、胶质潴留;大昔淋巴细胞浸润和结构破坏;滤泡上皮细胞凋亡数量增加(34.66±2.78//vs 5.1 1±0.62,P<0.01);总T4下降、TSH升高,无自身抗体产生;淋巴结和脾脏细胞对Tg刺激增殖实验呈阳性反应.脾脏细胞上清中IL-4水平无升高,而IFN-升γ高[(1.272±0.049 vs 1.139±0.025)ng/L,P<0.01];甲状腺组织中除了IL4外,IFN-γ、CXCL10、ICAM-1 mRNA表达升高(均P<0.01).而Tg组甲状腺内有少量散在淋巴细胞浸润,产生了甲状腺自身抗体,脾脏细胞上清中IL-4水平升高[(18.508±0.113绑13.368±0.016)ng/L,P<0.01].碘和Tg联合作用炎症反应加重.结论碘过量所致的NOD小鼠甲状腺炎主要是以Th1反应为主的器官特异性自身免疫性疾病.碘过量联合Tg免疫对诱发实验性自身免疫性甲状腺炎具有协同作用.
목적 관찰전과량화갑상선구단백(Tg)면역유발갑상선염적병변특점,진일보료해전과량재자신면역성갑상선염발병중적작용궤제.방법 선용NOD소서,음0.05%전화납(NaI)수화(혹)Tg피하면역.관찰갑상선형태학개변화세포조망정황;검측혈청중TT4、TSH、갑상선구단백항체(TgAb)화갑상선과양화물매항체(TPOAb)수평;검측경부림파결화비장림파세포대Tg자격적증식반응화비장세포배양상청중백세포개소4(IL-4)화1γ-간우소(IFN-γ)수평;실시형광정량PCR법검측갑상선감직내IL-4、IFN-γ、추화강자배체10(CXCL10)、세포간점부인자1(ICAM-1)mRNA적표체.결과 전과량조갑상선려포확장、효질저류;대석림파세포침윤화결구파배;려포상피세포조망수량증가(34.66±2.78//vs 5.1 1±0.62,P<0.01);총T4하강、TSH승고,무자신항체산생;림파결화비장세포대Tg자격증식실험정양성반응.비장세포상청중IL-4수평무승고,이IFN-승γ고[(1.272±0.049 vs 1.139±0.025)ng/L,P<0.01];갑상선조직중제료IL4외,IFN-γ、CXCL10、ICAM-1 mRNA표체승고(균P<0.01).이Tg조갑상선내유소량산재림파세포침윤,산생료갑상선자신항체,비장세포상청중IL-4수평승고[(18.508±0.113방13.368±0.016)ng/L,P<0.01].전화Tg연합작용염증반응가중.결론 전과량소치적NOD소서갑상선염주요시이Th1반응위주적기관특이성자신면역성질병.전과량연합Tg면역대유발실험성자신면역성갑상선염구유협동작용.
Objective To observe the pathological characteristics of thyroiditis induced by iodine excess and thyroglobulin (Tg) immunization and to explore the mechanism of thyroiditis induced by iodine excess. Methods NOD mice were used for intaking 0.05% Nal water and(or) Tg immunization. Morphologic change in thyroid and apoptosis were observed. The levels of serum TT4, TSH, thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) were measured. Responding to Tg, lymphocytic proliferation of lymph node and spleen, interleukin-4(IL-4)and γ-interferon(IFN-γ) levels in culture medium of splenocytes were detected. Real-time PCR Was used to detect mRNA expressions of IL-4, IFN-γ, chemokine ligand 10 (CXCL10) and intercellular adhesion molecular-1(ICAM-1) in thyroid. Results Distended thyroid follicles,colloid accumulation, intense lymphocytic infiltration and disorganization were seen in thyroid of iodine excess group, along with increased apoptosis of thyroid cells(34.66～ 2.78 vs 5.11±0.62 ,P<0.01). The levels of TT4 were lowered while TSH raised ,but no production of thyroid-specific autoantibodies was revealed. Lymph node and spleen cells showed positive respornse under stimulation of Tg. The level of IFN-γ[(1. 272±0.049 vs 1. 139±0. 025)ng/L,P<0. 01] was raised in culture medium of splenocytes but not IL-4. The expression of IFN-γ, CXCLI0 and ICAM-1 mRNA were increased in thyroid. But in Tg group, some lymphocytes were scattered in thyroid, autoantibodies emerged ,and the level of IL-4 was increased in cuhure medium of splenocytes[(18. 508±0. 113 vs 13. 368±0. 016)ng/L, P<0. 01]. ledine excess combined with Tg enhanced these inflammatory reaction. Conclusion Iodine excess induced thyroiditis in NOD mice. The process seems to be Th1 response dominant organ-specific autoimmune diseases. Iodine excess and Tg immunizatiou play a synergistic role in inducing experimental autoimmune thyroiditis.