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The Journal of Immunology, 2000, 164: 152-160.
Copyright © 2000 by The American Association of Immunologists

Effects of T3R{alpha}1 and T3R{alpha}2 Gene Deletion on T and B Lymphocyte Development1

Christophe Arpin2, Maria Pihlgren2, Alexandre Fraichard, Denise Aubert, Jacques Samarut, Olivier Chassande3 and Jacqueline Marvel3

Ecole Normale Supérieure de Lyon, Laboratoire de Biologie Moléculaire et Cellulaire, Unité Mixte de Recherche 5665 Centre National de la Recherche Scientifique/Ecole Normale Supérieure, Lyon, France

Thyroid hormones bind to several nuclear receptors encoded by T3R{alpha} and T3Rß genes. There is now accumulating evidence that thyroid hormones act on the immune system. Indeed, mice deficient for thyroid hormones show a reduction in lymphocyte production. However, the mechanisms involved and, in particular, the role of the different thyroid hormone receptors in lymphocyte development have not been investigated. To address that question, we have studied lymphocyte development in mice deficient for the T3R{alpha}1 and T3R{alpha}2 gene products. A strong decrease in spleen cell numbers was found compared with wild-type littermates, B lymphocytes being more severely affected than T lymphocytes. A significant decrease in splenic macrophage and granulocyte numbers was also found. In bone marrow, a reduction in CD45+/IgM- pro/pre-B cell numbers was found in these mice compared with wild-type littermates. This decrease seems to result from a proliferation defect, as CD45+/IgM- cells incorporate less 5-bromo-2'-deoxyuridine in vivo. To define the origin of the bone marrow development defect, chimeric animals between T3R{alpha}-/- and Rag1-/- mice were generated. Results indicate that for B cells the control of the population size by T3R{alpha}1 and T3R{alpha}2 is intrinsic. Altogether, these results show that T3R{alpha}1 or T3R{alpha}2 gene products are implicated in the control of the B cell pool size.




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