Hormonal Regulation of Tumor Necrosis Factor-α, Interleukin-12 and Interleukin-10 Production by Activated Macrophages: A Disease-modifying Mechanism in Rheumatoid Arthritis and Systemic Lupus Erythematosus?

Authors

  • RONALD L. WILDER,

    Corresponding author
    1. Inflammatory Joint Diseases Section, Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA
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  • ILIA J. ELENKOV

    1. Inflammatory Joint Diseases Section, Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA
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Address correspondence to Ronald L. Wilder, Chief, Inflammatory Joint Diseases Section, NIAMS, NIH, Bldg. 10, Room 9N228, 10 Center Drive, MSC 1820, Bethesda, MD 20892. Tel: 301-496-6499; fax: 301-402-0012; E-mail: wilderr@arb.niams.nih.gov

Abstract

ABSTRACT: Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) frequently develop and progress in settings in which sympathoadrenomedullary and gonadal hormone levels are changing, e.g., during pregnancy, postpartum period, menopause, estrogen administration. This paper addresses the view that adrenal and gonadal hormonal deficiency facilitates excessive macrophage production of TNF-α and IL-12 that characterizes RA, whereas excessive estrogen action is suggested to play an essential role in the production of IL-10 in patients with SLE. Disease activity in SLE, in contrast to RA, appears to be associated with high-level production of IL-10, relative to the proinflammatory cytokines, TNF-α and IL-12. Accumulating data suggest that novel therapeutic approaches may ultimately be developed from continued investigation of the role of the neuroendocrine factors in RA and SLE.

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