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Sökning: L773:1440 1711 OR L773:0818 9641 > Role of estrogen si...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005620naa a2200409 4500
001oai:gup.ub.gu.se/339083
003SwePub
008240911s2024 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/3390832 URI
0247 a https://doi.org/10.1111/imcb.127732 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Barrett, Aidanu Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research4 aut0 (Swepub:gu)xbarra
2451 0a Role of estrogen signaling in fibroblastic reticular cells for innate and adaptive immune responses in antigen-induced arthritis
264 1c 2024
520 a Women are more prone to develop rheumatoid arthritis, with peak incidence occurring around menopause. Estrogen has major effects on the immune system and is protective against arthritis. We have previously shown that treatment with estrogen inhibits inflammation and joint destruction in murine models of arthritis, although the mechanisms involved remain unclear. Fibroblastic reticular cells (FRCs) are specialized stromal cells that generate the three-dimensional structure of lymph nodes (LNs). FRCs are vital for coordinating immune responses from within LNs and are characterized by the expression of the chemokine CCL19, which attracts immune cells. The aim of this study was to determine whether the influence of estrogen on innate and adaptive immune cells in arthritis is mediated by estrogen signaling in FRCs. Conditional knockout mice lacking estrogen receptor alpha (ER alpha) in CCL19-expressing cells (Ccl19-CreER alpha fl/fl) were generated and tested. Ccl19-CreER alpha fl/fl mice and littermate controls were ovariectomized, treated with vehicle or estradiol and subjected to the 28-day-long antigen-induced arthritis model to enable analyses of differentiated T- and B-cell populations and innate cells in LNs by flow cytometry. The results reveal that while the response to estradiol treatment in numbers of FRCs per LN is significantly reduced in mice lacking ER alpha in FRCs, estrogen does not inhibit joint inflammation or markedly affect immune responses in this arthritis model. Thus, this study validates the Ccl19-CreER alpha fl/fl strain for studying estrogen signaling in FRCs within inflammatory diseases, although the chosen arthritis model is deemed unsuitable for addressing this question. This study investigated the influence of signaling through estrogen receptor alpha (ER alpha) in fibroblastic reticular cells (FRCs) on innate and adaptive immune responses using a mouse model where ER alpha was conditionally deleted in CCL19-expressing cells. The results reveal that the deletion of ER alpha in FRCs does not affect the FRC phenotype or LN architecture at steady state while the response of FRCs to estrogen treatment during experimental arthritis is significantly reduced in the conditional knock-out mice. However, ER alpha signaling via FRCs does not inhibit joint inflammation or markedly affect immune responses in the antigen-induced arthritis model. image
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
653 a Antigen-induced arthritis
653 a estrogen
653 a estrogen receptor alpha
653 a fibroblastic reticular cells
653 a lymph node
653 a inflammation
7001 a Horkeby, Karinu Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition4 aut0 (Swepub:gu)xgukab
7001 a Corciulo, Carmenu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology4 aut0 (Swepub:gu)xcorca
7001 a Carlsten, Hans,d 1954u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research4 aut0 (Swepub:gu)xcahan
7001 a Lagerquist, Marie Ku Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition4 aut0 (Swepub:gu)xlmarv
7001 a Scheffler, Julia,d 1982u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research4 aut0 (Swepub:gu)xscjul
7001 a Islander, Ulrika,d 1975u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research4 aut0 (Swepub:gu)xislul
7102 a Göteborgs universitetb Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning4 org
7730 t IMMUNOLOGY AND CELL BIOLOGYg 102:7, s. 578-592q 102:7<578-592x 0818-9641x 1440-1711
8564 8u https://gup.ub.gu.se/publication/339083
8564 8u https://doi.org/10.1111/imcb.12773

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