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Is Necessary in Thymic Development and Estradiol-Induced Thymic Alterations1
*
Department of Microbiology and Immunology, State University of New York Health Science Center, Syracuse, NY 13210;
Environmental Health Science Center, Department of Environmental Medicine, University of Rochester School of Medicine, Rochester, NY 14642;
Department of Biochemistry, University of Missouri, Columbia, MO 65211; and
§
Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental and Health Sciences, Research Triangle Park, NC 27709
Estrogens affect the development, maturation, and function of
multiple organ systems, including the immune system. One of the main
targets of estrogens in the immune system is the thymus, which
undergoes atrophy and phenotypic alterations when exposed to elevated
levels of estrogen. To determine how estrogens influence the thymus and
affect T cell development, estrogen receptor 
(ER) knockout
(ERKO) mice were examined. ERKO mice have significantly smaller thymi
than their wild-type (WT) littermates. Construction of ER radiation
bone marrow chimeras indicated that the smaller thymi were due to a
lack of ER in radiation-resistant tissues rather than hemopoietic
elements. ERKO mice were also susceptible to estradiol-induced thymic
atrophy, but the extent of their atrophy was less than what was seen in
WT mice. The estradiol-treated ERKO mice failed, however, to manifest
alterations in their thymic CD4/CD8 phenotypes compared with WT mice.
Therefore, ER is essential in nonhemopoietic cells to obtain a
full-sized thymus, and ER also mediates some of the response of the
thymus to elevated estrogen levels. Finally, these results suggest that
in addition to ER, another receptor pathway is involved in
estradiol-induced thymic atrophy.
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