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A brief description of my research

Rheumatic diseases are much more common in women than in men. For instance, 90% of patients with systemic lupus erythematosus (SLE) and 70% with rheumatoid arthritis (RA) are women. The female predominance has been attributed to sex hormones.

In earlier studies, Dr. Carlsten and coworkers demonstrated that estrogen exerts a dichotomous effect on the immune system by downregulating T-lymphocyte-mediated responses and augmenting immunoglobulin production. They were the first to demonstrate that estrogen- and testosterone-mediated suppression of T-cell-dependent inflammation is inherited as dominant traits. Using estrogenreceptor (ER) knock-out mice, they mapped the roles of ERα and ERβ in estrogen-mediated effects on the development and regulation of the immune system and on immune responsiveness. In murine models of autoimmune rheumatic diseases they revealed that physiological doses of estrogen accelerate SLE and ameliorate RA.

Currently, they are exploring the cellular and molecular mechanisms by which estrogen downregulates arthritis and preserves bone loss during systemic inflammation.

 In clinical studies of postmenopausal RA patients, Dr. Carlsten and coworkers have established that hormone replacement therapy (HRT) has beneficial effects not only on bone mineral density but also on disease activity and erosivity in joints. Since long-term use of HRT has been associated with increased risk of breast cancer, thrombosis, and possibly also stroke, they have focused on the possible use of selective estrogen receptor modulators (SERM) for treatment of arthritis.

Recently, they demonstrated that the selective estrogen receptor modifier raloxifene reduces joint destruction and bone loss triggered by arthritis and inflammation. They also demonstrated that the synthetic estrogen-like substance estren affects the immune system by signaling through both ERs and ARs.

Professor Hans Carlsten


Hans Carlsten

Box 480, 405 30 Göteborg

Guldhedsgatan 10 A

46 31 342 40 17

Sidansvarig: kommunikation@medicine.gu.se|Sidan uppdaterades: 2010-09-06

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