CAJ | 학술논문

目的：探讨异基因骨髓间充质干细胞（BM-MSC）对实验性自身免疫性甲状腺炎（EAT）的治疗作用及其机制。方法利用猪甲状腺球蛋白和弗氏佐剂免疫 C57BL/6小鼠，制备 EAT 小鼠模型。BM-MSC干预组小鼠在建模同时尾静脉输注同源 BM-MSC，每只3×105，每周1次，共4次。所有小鼠均在免疫后28 d 处死，分离甲状腺组织，石蜡切片、HE 染色后进行病理学分析；分离血清，放射免疫分析法检测甲状腺球蛋白抗体（TgAb）、甲状腺微粒体抗体（TmAb）、甲状腺过氧化物酶抗体（TPOAb）、总3，5，3'，5'-四碘甲腺原氨酸（TT4）、总3，5，3'-三碘甲腺原氨酸（TT3）、干扰素γ（lFN-γ）和白细胞介素10（lL-10）水平。结果①与正常对照组比较，模型组小鼠 TgAb，TmAb 和 TPOAb 均明显增高，TT4水平明显降低（P﹤0.05），TT3水平无明显差异，甲状腺组织破坏明显，提示成功建立 EAT 小鼠模型。②正常对照组甲状腺组织未见淋巴细胞浸润；模型组甲状腺组织淋巴细胞浸润明显；BM-MSC 干预组可见甲状腺组织淋巴细胞浸润，浸润程度较模型组减轻。③与正常对照组相比，模型组血清中 TgAb，TmAb，TPOAb 和 lFN-γ水平增高，lL-10水平降低（P﹤0.05）；BM-MSC 干预组与模型组相比，血清中 TgAb，TmAb 和 TPOAb 水平明显降低，TT4水平明显升高（P﹤0.05），TT3水平无明显差异，lFN-γ表达水平降低，lL-10表达水平增高（ P﹤0.05）。结论 BM-MSC 对 EAT 具有一定的治疗作用，其机制有可能与其调节辅助性 T 细胞（Th）1/ Th2免疫平衡有关。
목적：탐토이기인골수간충질간세포（BM-MSC）대실험성자신면역성갑상선염（EAT）적치료작용급기궤제。방법이용저갑상선구단백화불씨좌제면역 C57BL/6소서，제비 EAT 소서모형。BM-MSC간예조소서재건모동시미정맥수주동원 BM-MSC，매지3×105，매주1차，공4차。소유소서균재면역후28 d 처사，분리갑상선조직，석사절편、HE 염색후진행병이학분석；분리혈청，방사면역분석법검측갑상선구단백항체（TgAb）、갑상선미립체항체（TmAb）、갑상선과양화물매항체（TPOAb）、총3，5，3'，5'-사전갑선원안산（TT4）、총3，5，3'-삼전갑선원안산（TT3）、간우소γ（lFN-γ）화백세포개소10（lL-10）수평。결과①여정상대조조비교，모형조소서 TgAb，TmAb 화 TPOAb 균명현증고，TT4수평명현강저（P﹤0.05），TT3수평무명현차이，갑상선조직파배명현，제시성공건립 EAT 소서모형。②정상대조조갑상선조직미견림파세포침윤；모형조갑상선조직림파세포침윤명현；BM-MSC 간예조가견갑상선조직림파세포침윤，침윤정도교모형조감경。③여정상대조조상비，모형조혈청중 TgAb，TmAb，TPOAb 화 lFN-γ수평증고，lL-10수평강저（P﹤0.05）；BM-MSC 간예조여모형조상비，혈청중 TgAb，TmAb 화 TPOAb 수평명현강저，TT4수평명현승고（P﹤0.05），TT3수평무명현차이，lFN-γ표체수평강저，lL-10표체수평증고（ P﹤0.05）。결론 BM-MSC 대 EAT 구유일정적치료작용，기궤제유가능여기조절보조성 T 세포（Th）1/ Th2면역평형유관。
OBJECTIVE To investigate the curative effect and mechanism of allo-bone marrow mes-enchymal stem cell(BM-MSC)infusion in the experimental autoimmune thyroiditis(EAT)mouse model. METHODS An EAT mouse model was established in C57BL/ 6 mice using porcine thyroglobulin(PTg) and Freund adjuvant,while BM-MSCs were injected into the EAT mice of BM-MSC treated group,3×105 per mouse on the 0,7th,14th and 21st day. On the 28th day,all the mice were sacrificed,and thyroid tissue was isolated,embedded in paraffin and stained with HE staining for histological examination. Serum was collected to assess the level of thyroglobulin antibodies( TgAb ) ,thyroid microsomal autoantibodies( TmAb),antithyroid peroxidase antibodies( TPOAb),3,5,3 ',5 '-tetraiodothyronine (TT4),3,5,3 '-triiodothyronine( TT3),interleukin-10( lL-10) and interferon-γ( lFN-γ ). RESULTS① Thyroid tissue in model group showed inflammatory response and infiltration. The level of TmAb, TgAb and TPOAb was significantly increased compared with normal control group,but the level of TT4 was decreased while there was no change in the level of TT3,suggesting that an EAT mouse model was established. ② The thyroid in model group and BM-MSC treated group showed inflammatory response and inflammatory cell infiltration,but the response in BM-MSC treated group was weaker than in model group. ③ Compared with model group,the level of TgAb,TmAb,TPOAb and lFN-γ was decreased obvi-ously(P﹤0.05),the level of TT4 and lL-10 was increased significantly(P﹤0.05),but the level of TT3 changed little in BM-MSC treated group. CONCLUSION BM-MSCs may partly restore the immunologi-cal homeostasis state. The mechanism may be related to its modulation of immune balance of Th1/ Th2.