Dehydroepiandrosterone as a regulator of immune cell function

被引:114
作者
Hazeldine, Jon [1 ]
Arlt, Wiebke [2 ]
Lord, Janet M. [1 ]
机构
[1] Univ Birmingham, Sch Med, MRC, Ctr Immune Regulat,Sch Immun & Infect, Birmingham B15 2TT, W Midlands, England
[2] Univ Birmingham, Sch Med, Sch Clin & Expt Med, Birmingham B15 2TT, W Midlands, England
基金
英国生物技术与生命科学研究理事会;
关键词
DHEA; Ageing; Immunity; SYSTEMIC-LUPUS-ERYTHEMATOSUS; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; AGE-ASSOCIATED DECLINE; COLLAGEN-INDUCED ARTHRITIS; BLOOD MONONUCLEAR-CELLS; SEX STEROID-METABOLISM; NITRIC-OXIDE RELEASE; ORAL DEHYDROEPIANDROSTERONE; INFLUENZA VACCINATION; SULFATE CONCENTRATIONS;
D O I
10.1016/j.jsbmb.2009.12.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Dehydroepiandrosterone (DHEA) is a C19 steroid of adrenal origin. Notably, its secretion declines with age, a phenomenon referred to as the "adrenopause". For many years, the physiological significance of DHEA remained elusive. However, many studies have now shown that DHEA has significant immune modulatory function, exhibiting both immune stimulatory and anti-glucocorticoid effects. Although several of these studies are limited by the fact that they were carried out in rodents, who are incapable of adrenal DHEA production, and therefore have very low circulating levels of this steroid, evidence from the study of immune cells is now accumulating to suggest a role for DHEA in regulating human immunity. This ability to regulate immune function has raised interest in the therapeutic potential of DHEA as a treatment for the immunological abnormalities that arise in subjects with low circulating levels of this hormone. This has included attempts at reversing the impaired immune response of older individuals to vaccination and restoring immune regulation in patients with chronic autoimmune disease. This review summarises the reported effects of DHEA on immune function and discusses the therapeutic potential of this steroid in geriatric medicine and particularly in age-related disease with an immune component. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:127 / 136
页数:10
相关论文
共 128 条
[61]   Dehydroepiandrosterone activates endothelial cell nitric-oxide synthase by a specific plasma membrane receptor coupled to Gαi2,3 [J].
Liu, DM ;
Dillon, JS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (24) :21379-21388
[62]   Dehydroepiandrosterone stimulates nitric oxide release in vascular endothelial cells: evidence for a cell surface receptor [J].
Liu, DM ;
Dillon, JS .
STEROIDS, 2004, 69 (04) :279-289
[63]   Dehydroepiandrosterone stimulates endothelial proliferation and angiogenesis through extracellular signal-regulated kinase 1/2-mediated mechanisms [J].
Liu, Dongmin ;
Iruthayanathan, Mary ;
Homan, Laurie L. ;
Wang, Yiqiang ;
Yang, Lingling ;
Wang, Yao ;
Dillon, Joseph S. .
ENDOCRINOLOGY, 2008, 149 (03) :889-898
[64]   IN-VIVO PRODUCTION OF INTERLEUKIN-10 BY NON-T CELLS IN RHEUMATOID-ARTHRITIS, SJOGRENS-SYNDROME, AND SYSTEMIC LUPUS-ERYTHEMATOSUS - A POTENTIAL MECHANISM OF B-LYMPHOCYTE HYPERACTIVITY AND AUTOIMMUNITY [J].
LLORENTE, L ;
RICHAUDPATIN, Y ;
FIOR, R ;
ALCOCERVARELA, J ;
WIJDENES, J ;
FOURRIER, BM ;
GALANAUD, P ;
EMILIE, D .
ARTHRITIS AND RHEUMATISM, 1994, 37 (11) :1647-1655
[65]  
Longcope C, 1996, J ENDOCRINOL, V150, pS125
[66]   Metabolism of dehydroepiandrosterone [J].
Longcope, C .
DEHYDROEPIANDROSTERONE (DHEA) AND AGING, 1995, 774 :143-148
[67]   Immune up-regulation and tumor apoptosis by androstene steroids [J].
Loria, RM .
STEROIDS, 2002, 67 (12) :953-966
[68]   ANDROSTENEDIOL REGULATES SYSTEMIC RESISTANCE AGAINST LETHAL INFECTIONS IN MICE [J].
LORIA, RM ;
PADGETT, DA .
ARCHIVES OF VIROLOGY, 1992, 127 (1-4) :103-115
[69]   PROTECTION AGAINST ACUTE LETHAL VIRAL-INFECTIONS WITH THE NATIVE STEROID DEHYDROEPIANDROSTERONE (DHEA) [J].
LORIA, RM ;
INGE, TH ;
COOK, SS ;
SZAKAL, AK ;
REGELSON, W .
JOURNAL OF MEDICAL VIROLOGY, 1988, 26 (03) :301-314
[70]   HORMONAL AND PREGNANCY RELATIONSHIPS TO RHEUMATOID-ARTHRITIS - CONVERGENT EFFECTS WITH IMMUNOLOGICAL AND MICROVASCULAR SYSTEMS [J].
MASI, AT ;
FEIGENBAUM, SL ;
CHATTERTON, RT .
SEMINARS IN ARTHRITIS AND RHEUMATISM, 1995, 25 (01) :1-27