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Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104;
Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709; and
Departments of Biochemistry and Child Health, University of Missouri, Columbia, MO 65211
Several observations suggest that sex steroids might participate in
steady state regulation of B lymphopoiesis. B cell precursors decline
dramatically in bone marrow of pregnant or estrogen-treated mice.
Reciprocally, the same cell populations are increased in hypogonadal
mice or male castrates. Estrogen treatment of hypogonadal mice reduced
precursors to normal. However, questions remain about which hormones
and receptors are the most important. Furthermore, these observations
need to be reconciled with advances regarding new sex steroid
receptors. We have now characterized B lymphopoiesis in androgen
receptor-deficient testicular feminization
(Tfm) mice. Testicular feminization mice had
substantially elevated numbers of B cell precursors in the bone marrow
and B cells in the spleen as compared with wild-type mice. The
importance of one estrogen receptor (ER
) was evaluated in
gene-targeted mice, and B cell precursors were found to be within the
normal range. Our previous studies indicated that hormone receptors in
stromal cells may be important for estrogen-mediated suppression of B
lymphopoiesis. We now show that estrogen-mediated inhibition of B cell
precursor expansion in culture was blocked by a specific estrogen
receptor antagonist (ICI 182,780). Stromal cells derived from
ER-targeted bone marrow were fully estrogen responsive. RT-PCR
analyses of these stromal cells revealed splice-variant transcripts of
ER, as well as message for a recently discovered estrogen-binding
receptor, ERß. Thus, androgens may normally inhibit B lymphopoiesis
through the androgen receptor, whereas estrogens might utilize one or
more receptors to achieve the same physiologic response.
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