Increased B lymphopoiesis in genetically sex steroid-deficient hypogonadal (hpg) mice.
Interleukin 7 (IL-7) responsive B lineage precursors were greatly expanded in genetically hypogonadal female (HPG/Bm-hpg/hpg) mice that have a secondary deficiency in gonadal steroidogenesis. Estrogen replacement in these mice resulted in a dose-dependent reduction in B cell precursors. More modest increases were documented in genetically normal mice that were surgically castrated. These findings complement other recent observations that B lymphopoiesis selectively declines in pregnant or estrogen-treated animals. Sex steroids have long been known to influence such disparate processes as bone physiology and tumor growth, in addition to their importance for reproductive function. We now show that these hormones are important negative regulators of B lymphopoiesis.
Smithson
G
G
Oklahoma Medical Research Foundation, Oklahoma City 73104.
Beamer
W G
WG
Shultz
K L
KL
Christianson
S W
SW
Shultz
L D
LD
Kincade
P W
PW
D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology* / Q000276:immunology; D002455:Cell Division / Q000235:genetics; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000172:deficiency / Q000502:physiology* / Q000627:therapeutic use; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000235:genetics; D007006:Hypogonadism / Q000188:drug therapy / Q000235:genetics / Q000276:immunology*; D015851:Interleukin-7 / Q000502:physiology; D051379:Mice
D004967:Estrogens; D015851:Interleukin-7; D007987:Gonadotropin-Releasing Hormone