| First Author | Martin AP | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 5 | Pages | 3073-80 |
| PubMed ID | 19675158 | Mgi Jnum | J:151849 |
| Mgi Id | MGI:4355445 | Doi | 10.4049/jimmunol.0900275 |
| Citation | Martin AP, et al. (2009) CCR7 deficiency in NOD mice leads to thyroiditis and primary hypothyroidism. J Immunol 183(5):3073-80 |
| abstractText | 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 CCR7(ko/ko) mice (in which ko signifies deficient) onto the autoimmune-prone NOD background. Surprisingly, NODCCR7(ko/ko) mice never developed diabetes, but showed severe inflammation in multiple tissues including thyroid, lung, stomach, intestine, uterus, and testis. NODCCR7(ko/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 NODCCR7(ko/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 NODCCR7(ko/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. |
