| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Laboratory of Experimental Rheumatology and Neuroendocrino-Immunology, Division of Rheumatology, Department of Internal Medicine I, University Hospital, 93042 Regensburg, Germany
* To whom correspondence should be addressed. E-mail: rainer.straub{at}klinik.uni-regensburg.de.
There is still an unresolved paradox with respect to the immunomodulating role of estrogens. On one side, we recognize inhibition of bone resorption and suppression of inflammation in several animal models of chronic inflammatory diseases. On the other hand, we realize the immunosupportive role of estrogens in trauma/sepsis and the proinflammatory effects in some chronic autoimmune diseases in humans. This review examines possible causes for this paradox.
This review delineates how the effects of estrogens are dependent on criteria such as: 1) the immune stimulus (foreign antigens or autoantigens) and subsequent antigen-specific immune responses (e.g., T cell inhibited by estrogens vs. activation of B cell); 2) the cell types involved during different phases of the disease; 3) the target organ with its specific microenvironment; 4) timing of 17
-estradiol administration in relation to the disease course (and the reproductive status of a woman); 5) the concentration of estrogens; 6) the variability in expression of estrogen receptor 
and depending on the microenvironment and the cell type; and 7) intracellular metabolism of estrogens leading to important biologically active metabolites with quite different anti- and proinflammatory function. Also mentioned are systemic supersystems such as the hypothalamic-pituitary-adrenal axis, the sensory nervous system, and the sympathetic nervous system and how they are influenced by estrogens.
This review reinforces the concept that estrogens have antiinflammatory but also proinflammatory roles depending on above-mentioned criteria. It also explains that a uniform concept as to the action of estrogens cannot be found for all inflammatory diseases due to the enormous variable responses of immune and repair systems.
This article has been cited by other articles:
 |
|
 |
|
  Z. OuYang, Y. Hirota, Y. Osuga, K. Hamasaki, A. Hasegawa, T. Tajima, T. Hirata, K. Koga, O. Yoshino, M. Harada, et al. Interleukin-4 Stimulates Proliferation of Endometriotic Stromal Cells Am. J. Pathol., August 1, 2008; 173(2): 463 - 469. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N.M. Nowak, O.M. Fischer, T.C. Gust, U. Fuhrmann, U.-F. Habenicht, and A. Schmidt Intraperitoneal inflammation decreases endometriosis in a mouse model Hum. Reprod., July 24, 2008; (2008) den189v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Gorjestani, V Rider, B. Kimler, C Greenwell, and N. Abdou Extracellular signal-regulated kinase 1/2 signalling in SLE T cells is influenced by oestrogen and disease activity Lupus, June 1, 2008; 17(6): 548 - 554. [Abstract] [PDF]
|
|
|
|
 |
|
 V. M. Miller and S. P. Duckles Vascular Actions of Estrogens: Functional Implications Pharmacol. Rev., June 1, 2008; 60(2): 210 - 241. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Cutolo, S. Capellino, and R. H. Straub Oestrogens in rheumatic diseases: friend or foe? Rheumatology, June 1, 2008; 47(suppl_3): iii2 - iii5. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
