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Effects of a tissue-selective estrogen complex on B lymphopoiesis and B cell function

Journal article
Authors Jauqueline Nordqvist
Angelina I Bernardi
Ulrika Islander
Hans Carlsten
Published in Immunobiology
Volume 222
Issue 8-9
Pages 918-923
ISSN 0171-2985
Publication year 2017
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 918-923
Language en
Keywords Bazedoxifene, Estradiol, SERM, Tissue-selective estrogen complex (TSEC), Lymphopoiesis, Antibody production, receptor modulators, vasomotor symptoms, osteoporosis prevention, postmenopausal women, bazedoxifene, inflammation, arthritis, risk, bone, mice, Immunology, rkowski a, 1984, journal of immunological methods, v72, p451
Subject categories Rheumatology and Autoimmunity


Background/objective: 17 beta-estradiol (E2) has major effects on the immune system. It induces thymic atrophy, inhibits both T and B lymphopoiesis and stimulates antibody production treatment with E2 has protective effects on the skeleton but is associated with negative side effects in reproductive organs. A tissue-selective estrogen complex (TSEC) comprise of estrogens combined with a selective estrogen receptor modulator (SEEM). TSEC therapy displays the bone-protective effects of estrogen, while the negative side effects on reproductive organs are blocked by the SERM. In a recent publication we showed that treatment with the TSEC E2 + bazedoxifene (bza) potently inhibits experimental arthritis and associated osteoporosis. In order to elucidate immunological mechanisms involved in those effects, the aim of this study was to investigate how E2 + bza treatment affects the healthy immune system. Methods: Ovariectomized C57BL/6N mice were treated with vehicle, E2, bza or E2 + bza. Weights of uterus and thymus were determined and fluorescence-activated cell sorting was used to analyze B cell populations in bone marrow and spleen. Immunoglobulin production from B cells in bone marrow and spleen were determined using ELISPOT. Results: Addition of bza to E2-treatment totally antagonized the E2-mediated proliferative effect on uterus. On the contrary, addition of bza to E2-treatment did not block the E2-induced thymic atrophy or inhibition of B lymphopoiesis, and did not block the E2-induced increase in immunoglobulin secretion from bone marrow B cells. Conclusions: Addition of bza to E2-treatment blocks E2-induced uteroproliferation but does not alter E2-mediated effects on thymus, B lymphopoiesis or B cell function.

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