Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-1-19
pubmed:abstractText
Thyroid hormones bind to several nuclear receptors encoded by T3R alpha and T3R beta 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
152-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10605006-Animals, pubmed-meshheading:10605006-Animals, Newborn, pubmed-meshheading:10605006-B-Lymphocytes, pubmed-meshheading:10605006-Bone Marrow Cells, pubmed-meshheading:10605006-Cell Differentiation, pubmed-meshheading:10605006-Cell Division, pubmed-meshheading:10605006-DNA Nucleotidyltransferases, pubmed-meshheading:10605006-Gene Deletion, pubmed-meshheading:10605006-Integrases, pubmed-meshheading:10605006-Lymphocyte Count, pubmed-meshheading:10605006-Lymphoid Tissue, pubmed-meshheading:10605006-Lymphopenia, pubmed-meshheading:10605006-Mice, pubmed-meshheading:10605006-Mice, Knockout, pubmed-meshheading:10605006-Mice, Transgenic, pubmed-meshheading:10605006-Receptors, Thyroid Hormone, pubmed-meshheading:10605006-Recombinases, pubmed-meshheading:10605006-Spleen, pubmed-meshheading:10605006-Stem Cells, pubmed-meshheading:10605006-T-Lymphocytes, pubmed-meshheading:10605006-Triiodothyronine
pubmed:year
2000
pubmed:articleTitle
Effects of T3R alpha 1 and T3R alpha 2 gene deletion on T and B lymphocyte development.
pubmed:affiliation
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.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't