Humoral and cell-mediated immunity in mice with genetic deficiencies of prolactin, growth hormone, insulin-like growth factor-I, and thyroid hormone

被引:48
作者
Foster, MP
Jensen, ER
Montecino-Rodriguez, E
Leathers, H
Horseman, N
Dorshkind, K
机构
[1] Univ Calif Los Angeles, Sch Med, Dept Pathol & Lab Med 173216, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Sch Med, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA
[4] Univ Cincinnati, Coll Med, Dept Mol & Cellular Physiol, Cincinnati, OH 45267 USA
[5] Univ Cincinnati, Coll Med, Shriners Burns Inst, Cincinnati, OH 45267 USA
关键词
hormones; immunity; aging; hormone-deficient mice;
D O I
10.1006/clim.2000.4889
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Prolactin (PRL), growth hormone (GH), insulin-like growth factor-I (IGF-I), and thyroid hormones have been proposed as critical immunoregulatory mediators, and their clinical use is being considered. The precise role played by each of these hormones in the generation of humoral and cell-mediated immune responses was assessed in a panel of mice with mutations that result in a selective reduction of PRL, GH, IGF-I, and/or thyroid hormone production. A surprising result, in view of previous studies indicating an immunoregulatory role for these hormones, was that all mice generated normal humoral and cell-mediated immune responses following challenge with T-independent and T-dependent antigens and with Listeria monocytogenes. A review of these findings in the context of previous data has resulted in the formulation of a working hypothesis proposing that these hormones act as anabolic and/or stress modulating mediators with effects on most cells, including those of the immune system. When considered in this context, it is possible to reconcile the contradictory data. (C) 2000 Academic Press.
引用
收藏
页码:140 / 149
页数:10
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