Androgens Alter B Cell Development in Normal Male Mice

Viselli, Susan M.; Reese, Kevin; Jin, Fan; Kovacs, William J.; Olsen, Nancy J.

doi:10.1006/cimm.1997.1227

Cited by 114 publications

(91 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The suppressive effects of testosterone on immune function are widely accepted; however, the mechanism for this androgen control of immunity is not well understood. Both in vivo and in vitro testosterone exposure results in decreases in B and T lymphocyte expansion in the bone marrow, spleen, and thymus (Weinstein & Berkovich 1981, Olsen et al 1994, Olsen & Kovacs 1996, Viselli et al 1997. Burn injury is also known to alter splenocyte subpopulations within these organs (Kupper et al 1985, O'Mahony et al 1985, which could influence the DTH and splenocyte proliferative responses.…”

Section: Discussionmentioning

confidence: 99%

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

Messingham¹,

Shirazi²,

Duffner³

et al. 2001

Journal of Endocrinology

View full text Add to dashboard Cite

Males are known to have increased risk for septic complications after traumatic injury, which appears to be mediated by the inhibitory effects of testosterone on immune function. The role of testosterone in immunity after burn injury, however, remains unclear. Herein, we examined the effects of a testosterone receptor antagonist, flutamide, on delayed type hypersensitivity response (DTH), splenocyte proliferation, interleukin (IL)-2 secretion, and IL-2 receptor (IL-2R) expression in male BALB/c mice subjected to a 15% total body surface area burn or sham injury. Burn-or sham-injured mice were given flutamide s.c. at 30 min and 24 h after injury. At 48 h, burn injury caused a 48% (P<0·001) decrease in DTH response; however, mice that received flutamide treatment did not demonstrate significant suppression of DTH. Likewise, splenocyte proliferation and IL-2 production were depressed in burned animals in comparison with sham-injured controls, and flutamide treatment resulted in a partial restoration of these responses. In vitro studies indicated that splenocytes from sham-and burninjured mice were equally sensitive to the suppressive effects of 5 -dihydrotestosterone in regard to proliferation and IL-2 production. Further evaluation revealed a decrease in IL-2R expression on splenocytes from burned mice and a partial restoration of this expression with flutamide treatment. Thus blocking testosterone receptor activation improves the cellular immunity in thermally injured mice, possibly through restoration of IL-2 production and IL-2R expression. It remains to be determined whether the effects of testosterone in this injury model are direct or indirect.

show abstract

Section: Discussionmentioning

confidence: 99%

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

Messingham¹,

Shirazi²,

Duffner³

et al. 2001

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…These results suggest that the influences of endogenous estrogen can be ablated by using the G-CSF-TmR/Tm or delta G-CSF-TmR/ Tm system to expand hematopoietic stem cells with potential therapeutic application (65). Androgens exert an inhibitory effect on B lymphopoiesis (66,67), but enhance erythropoietic differentiation (68) and thrombocytopoiesis (69). Cultures of human erythropoietic precursor cells collected from children's normal marrow in the presence of erythropoietin demonstrated a significant increase in the number of colony-forming units (CFU-E) and burst-forming units (BFU-E) of derived colonies in the presence of androgens (10 (-8) M or 10 (-7) M).…”

Section: Hematopoietic Stem Cellsmentioning

confidence: 99%

Sex Steroids and Stem Cell Function

Ray

Novotny

Crisostomo

et al. 2008

Mol Med

104

View full text Add to dashboard Cite

Gender dimorphisms exist in the pathogenesis of a variety of cardiovascular, cardiopulmonary, neurodegenerative, and endocrine disorders. Estrogens exert immense influence on myocardial remodeling following ischemic insult, partially through paracrine growth hormone production by bone marrow mesenchymal stem cells (MSCs) and endothelial progenitor cells. Estrogens also facilitate the mobilization of endothelial progenitor cells to the ischemic myocardium and enhance neovascularization at the ischemic border zone. Moreover, estrogens limit pathological myocardial remodeling through the inhibitory effects on the proliferation of the cardiac fibroblasts. Androgens also may stimulate endothelial progenitor cell migration from the bone marrow, yet the larger role of androgens in disease pathogenesis is not well characterized. The beneficial effects of sex steroids include alteration of lipid metabolism in preadipocytes, modulation of bone metabolism and skeletal maturation, and prevention of osteoporosis through their effects on osteogenic precursors. In an example of sex steroid-specific effects, neural stem cells exhibit enhanced proliferation in response to estrogens, whereas androgens mediate inhibitory effects on their proliferation. Although stem cells can offer significant therapeutic benefits in various cardiovascular, neurodegenerative, endocrine disorders, and disorders of bone metabolism, a greater understanding of sex hormones on diverse stem cell populations is required to improve their ultimate clinical efficacy. In this review, we focus on the effects of estrogen and testosterone on various stem and progenitor cell types, and their relevant intracellular mechanisms.

show abstract

“…This raises the possibility that an altered cytokine pattern by immune cells induced by androgen deficiency may interact with marrow stromal cells, osteoblasts, and osteoclasts in the bone microenvironment (147). The significance of these findings on bone metabolism, however, remains to be defined.…”

Section: Other Factorsmentioning

confidence: 99%

Androgen effects on bone metabolism: recent progress and controversies

Hofbauer

Khosla

1999

European Journal of Endocrinology

122

View full text Add to dashboard Cite

Androgens have beneficial effects on skeletal development and maintenance in women and men. The detection and functional characterization of androgen receptors in bone cells has implicated bone tissue as a potential target tissue for androgens. Gonadal and adrenal androgens directly regulate various aspects of osteoblastic lineage cells, including proliferation, differentiation, mineralization, and gene expression. These effects may differ depending on the stage of differentiation, the number of androgen receptors, and other inherent characteristics (species, site, cell biology) of the osteoblastic cell system. In addition, recent studies have suggested that some of the anabolic and anti-resorptive effects of androgens on bone may be mediated by regulation of autocrine and paracrine factors in the bone microenvironment, including transforming growth factor-b, insulin-like growth factors (and their binding proteins), and interleukin-6. This review summarizes the recent progress made in our knowledge of androgen receptor action, local androgen metabolism in bone, and direct and indirect effects of gonadal and adrenal androgens as well as androgen receptor antagonists on bone cells.

show abstract

Androgens Alter B Cell Development in Normal Male Mice

Cited by 114 publications

References 26 publications

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

Testosterone receptor blockade restores cellular immunity in male mice after burn injury

Sex Steroids and Stem Cell Function

Androgen effects on bone metabolism: recent progress and controversies

Contact Info

Product

Resources

About