甲状腺球蛋白
甲状腺
点头
甲状腺炎
内分泌学
内科学
点头老鼠
自身免疫性甲状腺炎
自身免疫
医学
自身抗体
甲状腺肿
免疫学
免疫系统
糖尿病
抗体
作者
Andrea P. Martin,Tatjana Marinković,Claudia Canasto‐Chibuque,Rauf Latif,Jay C. Unkeless,Terry F. Davies,Yousuke Takahama,Gláucia C. Furtado,Sérgio A. Lira
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2009-08-12
卷期号:183 (5): 3073-3080
被引量:42
标识
DOI:10.4049/jimmunol.0900275
摘要
Abstract CCR7 is involved in the initiation of immune responses and has been recently implicated in the control of tolerance. To analyze the role of CCR7 in autoimmunity, we backcrossed CCR7ko/ko mice (in which ko signifies deficient) onto the autoimmune-prone NOD background. Surprisingly, NODCCR7ko/ko mice never developed diabetes, but showed severe inflammation in multiple tissues including thyroid, lung, stomach, intestine, uterus, and testis. NODCCR7ko/ko mice had a marked enlargement of the thyroid gland (goiter) that was associated with circulating autoantibodies against thyroglobulin, and development of primary hypothyroidism (decreased levels of serum thyroxin, and augmented levels of thyroid-stimulating hormone in the pituitary gland), features found in Hashimoto’s thyroiditis. Cells isolated from diseased thyroids and activated splenocytes from NODCCR7ko/ko animals induced goiter in NOD.SCID recipients, demonstrating that autoreactive cells were generated in the absence of CCR7. Moreover, thyroid disease could be accelerated in young NODCCR7ko/ko mice by immunization with thyroglobulin. These results demonstrate the complexity in the generation of multiple autoimmune phenotypes in NOD mice and indicate that CCR7 is a key molecule in their development.
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