Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-12-25
pubmed:abstractText
The thyroid hormones T(3) (tri-iodothyronine) and T(4) (thyroxine) are disseminated throughout the body via the circulation and are maintained across a range of physiological concentrations under the control of thyroid-stimulating hormone (TSH). T(3) (and T(4) after conversion to T(3)) influences many biological activities, including gene expression and protein synthesis, though little is known about the nature of pituitary-thyroid immune interactions. In the present study we show that serum T(3) and T(4) levels are sharply but transiently reduced during the first 24 h of systemic antigen exposure and that this is followed by suppressed levels of free T(4), after which there is rapid recovery to normal levels. Splenic dendritic cells, depending upon the stage of maturation/activation, were found to be a rich source of TSH, and CD11c(+) cells with dendritic cell morphology were present in the thyroid 1-3 days after antigen exposure. Moreover, antigen priming of hypophysectomized mice that are unable to make pituitary-derived TSH resulted in significant increases in circulating T(4), implying that compensation in the drop in thyroid hormones can be regulated from extrapituitary sources. These findings thus identify a novel set of immune-endocrine interactions that transpire during the early phase of antigen exposure, and they suggest that under appropriate conditions the immune system directly participates in the process of maintaining physiological homeostasis by contributing to the regulatory control of thyroid hormone activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
212
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
92-100
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11748925-Animals, pubmed-meshheading:11748925-Cell Movement, pubmed-meshheading:11748925-Chickens, pubmed-meshheading:11748925-Dendritic Cells, pubmed-meshheading:11748925-Disease Models, Animal, pubmed-meshheading:11748925-Euthyroid Sick Syndromes, pubmed-meshheading:11748925-Female, pubmed-meshheading:11748925-Hypophysectomy, pubmed-meshheading:11748925-Isoantigens, pubmed-meshheading:11748925-Mice, pubmed-meshheading:11748925-Mice, Inbred BALB C, pubmed-meshheading:11748925-Mice, Inbred C57BL, pubmed-meshheading:11748925-Mice, Transgenic, pubmed-meshheading:11748925-Muramidase, pubmed-meshheading:11748925-Neuroimmunomodulation, pubmed-meshheading:11748925-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:11748925-Secretory Rate, pubmed-meshheading:11748925-Spleen, pubmed-meshheading:11748925-Thyroid Gland, pubmed-meshheading:11748925-Thyrotropin, pubmed-meshheading:11748925-Thyroxine, pubmed-meshheading:11748925-Triiodothyronine
pubmed:year
2001
pubmed:articleTitle
Rapid and transient reduction in circulating thyroid hormones following systemic antigen priming: implications for functional collaboration between dendritic cells and thyroid.
pubmed:affiliation
Department of Biological Science, The University of Tulsa, Tulsa, Oklahoma 74104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't