Scheffler JM, Grahnemo L, Engdahl C, Drevinge C, Gustafsson KL, Corciulo C, Lawenius L, Iwakura Y, Sjögren K, Lagerqvist MK, Carlsten H, Ohlsson C, Islander U
Interleukin-17A: a Janus-faced regulator of osteoporosis
Sci Rep. 2020 Mar 30;10(1):5692.
Results from this study show that IL-17A is an important mediator of cortical but not trabecular bone loss after ovariectomy. Also, IL-17A induces a two-sided effect on bone remodelling in the absence of estrogen, by increasing osteoclastogenesis and decreasing adipogenesis
Andersson A, Törnqvist A, Moverare-Skrtic S, Bernardi A, Farman HH, Krust A, Chambon P, Engdahl C, Lagerquist M, Windahl SH, Carlsten H, Ohlsson C, Islander U
Roles of activating functions 1 and 2 of estrogen receptor a in estrogen receptor-mediated regulation of lymphopoiesis
J Endocrinol. 2018 Feb;236(2):99-109
This is the first study to establish in detail that the presence of activating functions 1-2 of estrogen receptor alpha (ERαAF-1 and ERαAF-2) are required for the effects that estradiol and selective estrogen receptor modulators (lasofoxifene and raloxifene) confer on the development of B- and T-lymphocytes in bone marrow and thymus.
Andersson A, Bernardi A, Nurkkala-Karlsson M, Stubelius A, Ohlsson C, Carlsten H, Islander U
Suppression of experimental arthritis and associated bone loss by a tissue-selective estrogen complex
Endocrinology. 2016 Jan 8:en20151820.
This paper shows that a tissue-selective estrogen complex, comprising estradiol and the selective estrogen receptor modulator Bazedoxifene, suppresses experimental arthritis and prevents associated bone loss in a manner that is equally efficient to that of estradiol alone, albeit with minimal uteroproliferative effects.
Andersson A, Stubelius A, Nurkkala Karlsson M, Engdahl C, Erlandsson MC, Grahnemo L, Lagerquist MK, Islander U
Estrogen regulates T helper 17 phenotype and localization in experimental autoimmune arthritis
Arthritis Res Ther. 2015 Feb 13;17:32.
This is the first study to characterize the effects of estradiol on Th17 cells in experimental autoimmune arthritis. We report that while estradiol treatment results in an increase in the numbers of Th17 cells in lymph nodes during the early phase of arthritis development, it also leads to a decrease in the numbers of Th17 cells in joints during established arthritis. Our data suggest that this may be caused by interference with the CCR6-CCL20 migration pathway, which is important for Th17-cell migration.