A novel model for lymphocytic infiltration of the thyroid gland generated by transgenic expression of the CC chemokine CCL21

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Item Type:	Article
Title:	A novel model for lymphocytic infiltration of the thyroid gland generated by transgenic expression of the CC chemokine CCL21
Creators Name:	Martin, A.P., Coronel, E.C., Sano, G., Chen, S.C., Vassileva, G., Canasto-Chibuque, C., Sedgwick, J.D., Frenette, P.S., Lipp, M., Furtado, G.C. and Lira, S.A.
Abstract:	Lymphocytic infiltrates and lymphoid follicles with germinal centers are often detected in autoimmune thyroid disease (AITD), but the mechanisms underlying lymphocyte entry and organization in the thyroid remain unknown. We tested the hypothesis that CCL21, a chemokine that regulates homeostatic lymphocyte trafficking, and whose expression has been detected in AITD, is involved in the migration of lymphocytes to the thyroid. We show that transgenic mice expressing CCL21 from the thyroglobulin promoter (TGCCL21 mice) have significant lymphocytic infiltrates, which are topologically segregated into B and T cell areas. Although high endothelial venules expressing peripheral lymph node addressin were frequently observed in the thyroid tissue, lymphocyte recruitment was independent of L-selectin or lymphotoxin-α but required CCR7 expression. Taken together, these results indicate that CCL21 is sufficient to drive lymphocyte recruitment to the thyroid, suggest that CCL21 is involved in AITD pathogenesis, and establish TGCCL21 transgenic mice as a novel model to study the formation and function of lymphoid follicles in the thyroid.
Keywords:	Adoptive Transfer, CC Chemokines, Cell Movement, Chemokine Receptors, Inbred C57BL Mice, Inbred DBA Mice, L-Selectin, Lymphocytes, Lymphotoxin-alpha, Transgenic Mice, Thyroid Diseases, Thyroid Gland, Animals, Mice, Rats
Source:	Journal of Immunology
ISSN:	0022-1767
Publisher:	American Association of Immunologists
Volume:	173
Number:	8
Page Range:	4791-4798
Date:	15 October 2004
Official Publication:	https://doi.org/10.4049/jimmunol.173.8.4791
PubMed:	View item in PubMed

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