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Titolo:
Estrogen, prolactin, and autoimmunity: actions and interactions
Autore:
McMurray, RW;
Indirizzi:
Univ Mississippi, Med Ctr, Dept Med, Div Rheumatol & Mol Immunol, Jackson,MS 39216 USA Univ Mississippi Jackson MS USA 39216 & Mol Immunol, Jackson,MS 39216 USA GV Sonny Montgomery VA Hosp, Rheumatol Sect, Jackson, MS 39216 USA GV Sonny Montgomery VA Hosp Jackson MS USA 39216 t, Jackson, MS 39216 USA
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 6, volume: 1, anno: 2001,
pagine: 995 - 1008
SICI:
1567-5769(200106)1:6<995:EPAAAA>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTEMIC-LUPUS-ERYTHEMATOSUS; B/W MOUSE MODEL; MULTIPLE-SCLEROSIS; SEX-HORMONES; GROWTH-HORMONE; RHEUMATOID-ARTHRITIS; DISEASE-ACTIVITY; CELL-LINES; IN-VITRO; IMMUNE-SYSTEM;
Keywords:
estrogen; prolactin; autoimmunity;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
138
Recensione:
Indirizzi per estratti:
Indirizzo: McMurray, RW Univ Mississippi, Med Ctr, Dept Med, Div Rheumatol & Mol Immunol, L525 Clin Sci Bldg, Jackson, MS 39216 USA Univ Mississippi L525 Clin Sci Bldg Jackson MS USA 39216 USA
Citazione:
R.W. McMurray, "Estrogen, prolactin, and autoimmunity: actions and interactions", INT IMMUNO, 1(6), 2001, pp. 995-1008

Abstract

Estrogen and prolactin have a reciprocal endocrinologic relationship and both hormones have pleiotropic effects on the immune system. Despite the presence of a number of confounding variables, these hormones modulate autoimmunity; however, mechanisms by which this modulation occurs remain obscure. Estrogen appears to suppress cell-mediated and augment humoral-based immunity. Prolactin appears to stimulate both cell and humoral-based immunity. Both hormones have been shown to modulate IFN gamma secretion. Similar evidence in experimental models, human autoimmune disease, and during pregnancy in autoimmune disease patients suggests disparate effects of estrogen and prolactin on autoimmune responses and disease pathogenesis. In the NZB X NZW F1 mouse model of lupus, prolactin accelerates disease expression, whereas estrogen, devoid of its prolactin stimulating properties, is immunosuppressive and inhibits IL-2 production. Estrogen, because of its endocrinologic and immune effects, may directly or indirectly stimulate or inhibit immune responses. These dichotomous effects have limited its successful pharmacologic manipulation in human autoimmune disease with estrogen compounds, tamoxifen, oral contraceptives, antigonadotropic agents, or ovulation induction regimens. In contrast, reduction of immunostimulatory concentrations of prolactin with bromocriptine has successfully suppressed development or expression of murine and human autoimmune disease. Further investigation into actions and interactions of estrogen and prolactin with autoimmunity will provide a better understanding of the female preponderance of autoimmunity and facilitate a more rational approach to hormonal immunotherapy. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 08:34:27