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Regenerative Potentials of the Murine Thyroid in Experimental Autoimmune Thyroiditis: Role of CD24

Department of Pathology (C.Y.C., H.K., M.A.L.-S., J.H., M.K., W.W., N.R.R., P.C.), The Johns Hopkins Medical Institutions, and Feinstone Department of Molecular Microbiology and Immunology (N.R.R., P.C.), The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205; and Department of Bioregulation (K.S.), Leprosy Research Center, National Institute of Infectious Diseases, Tokyo 189-0002, Japan

Address all correspondence and requests for reprints to: Patrizio Caturegli, Johns Hopkins Medical Institutions, Department of Pathology, Ross Building, Room 632, 720 Rutland Avenue, Baltimore, Maryland 21205. E-mail: pcat{at}jhmi.edu.

Hashimoto thyroiditis can be partially reproduced in mice by immunization with thyroglobulin or, more recently, thyroperoxidase. This experimental autoimmune thyroiditis (EAT) model has been extensively characterized during early disease phases (up to d 35 after immunization). By extending the analysis of EAT to 100 d after immunization, we noted a remarkable regenerative capacity of the thyroid and the expression of Oct-4, suggesting in vivo the existence of adult thyroid stem cells. After an almost complete destruction of the follicular architecture, occurring between d 21 and 28, the thyroid was capable of restoring its follicles and reducing the mononuclear infiltration, so that by d 100 after immunization, it regained its normal morphology and function. During this regeneration process, thyrocytes expressed high levels of CD24. We therefore assessed the role of CD24 in thyroid regeneration by inducing EAT in mice lacking CD24. Regeneration was faster in the absence of CD24, likely a consequence of the effect of CD24 on the infiltrating lymphocytes. The study suggests that the EAT model can also be used as a tool to investigate adult thyroid stem cells.

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