Androgens alter B cell development in normal male mice

S. M. Viselli, K. R. Reese, J. Fan, William Kovacs, Nancy Olsen

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Castration of normal male mice leads to splenic enlargement and expansion of the B cell population. Since the spleen does not express receptors for androgens, these changes are most likely mediated by effects of androgens on other target organs. Two potential sites of androgen-mediated effects on B cells are evaluated in these studies: thymus and bone marrow. We first confirmed other findings indicating that castration of normal male mice results in expansion in the numbers of bone marrow B cells and then extended these observations by showing that these changes were reversible following androgen replacement B cell expansion in castrate marrow and spleen was not altered by prior thymectomy, suggesting that thymic androgen receptors are not involved in the observed effects. Androgen receptors were found to be present in both immature B cells and marrow stromal cells by immunoblotting and ligand binding assays. The results suggest a direct modulatory role for androgens on B cells within the bone marrow compartment.

Original languageEnglish (US)
Pages (from-to)99-104
Number of pages6
JournalCellular Immunology
Volume182
Issue number2
DOIs
StatePublished - Dec 15 1997

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Androgens
B-Lymphocytes
Androgen Receptors
Bone Marrow
Orchiectomy
Spleen
Thymectomy
B-Lymphoid Precursor Cells
Stromal Cells
Immunoblotting
Bone Marrow Cells
Thymus Gland
Ligands
Population

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

Viselli, S. M. ; Reese, K. R. ; Fan, J. ; Kovacs, William ; Olsen, Nancy. / Androgens alter B cell development in normal male mice. In: Cellular Immunology. 1997 ; Vol. 182, No. 2. pp. 99-104.
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Androgens alter B cell development in normal male mice. / Viselli, S. M.; Reese, K. R.; Fan, J.; Kovacs, William; Olsen, Nancy.

In: Cellular Immunology, Vol. 182, No. 2, 15.12.1997, p. 99-104.

Research output: Contribution to journalArticle

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