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Estrogen regulates T helper 17 phenotype and localization in experimental autoimmune arthritis

Artikel i vetenskaplig tidskrift
Författare Annica Andersson
Alexandra Stubelius
Merja Nurkkala Karlsson
Cecilia Engdahl
Malin Erlandsson
Louise Grahnemo
Marie K Lagerquist
Ulrika Islander
Publicerad i Arthritis Research & Therapy
Volym 17
Nummer/häfte 32
ISSN 1478-6354
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Centre for Bone and Arthritis Research
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Språk en
Länkar dx.doi.org/10.1186/s13075-015-0548-...
Ämnesord COLLAGEN-INDUCED ARTHRITIS, HUMAN TH17 CELLS, RHEUMATOID-ARTHRITIS, RECEPTOR-ALPHA, MEDIATED INHIBITION, JOINT DESTRUCTION, GENE-EXPRESSION, MURINE MODEL, OSTEOPOROSIS, ENCEPHALOMYELITIS, Rheumatology
Ämneskategorier Reumatologi och inflammation

Sammanfattning

Introduction: The incidence and progression of many autoimmune diseases are sex-biased, which might be explained by the immunomodulating properties of endocrine hormones. Treatment with estradiol potently inhibits experimental autoimmune arthritis. Interleukin-17-producing T helper cells (Th17) are key players in several autoimmune diseases, particularly in rheumatoid arthritis. The aim of this study was to investigate the effects of estrogen on Th17 cells in experimental arthritis. Methods: Ovariectomized DBA/1 mice treated with 17 beta-estradiol (E2) or placebo were subjected to collagen-induced arthritis (CIA), and arthritis development was assessed. Th17 cells in joints and lymph nodes were studied by flow cytometry. Lymph node Th17 cells were also examined in ovariectomized estrogen receptor a-knockout mice (ERa-/-) and wild-type littermates, treated with E2 or placebo and subjected to antigen-induced arthritis. Results: E2-treated mice with established CIA showed reduced severity of arthritis and fewer Th17 cells in joints compared with controls. Interestingly, E2-treated mice displayed increased Th17 cells in lymph nodes during the early phase of the disease, dependent on ER alpha. E2 increased the expression of C-C chemokine receptor 6 (CCR6) on lymph node Th17 cells as well as the expression of the corresponding C-C chemokine ligand 20 (CCL20) within lymph nodes. Conclusions: This is the first study in which the effects of E2 on Th17 cells have been characterized in experimental autoimmune arthritis. We report that E2 treatment results in an increase of Th17 cells in lymph nodes during the early phase of arthritis development, but leads to a decrease of Th17 in joints during established arthritis. Our data suggest that this may be caused by interference with the CCR6-CCL20 pathway, which is important for Th17 cell migration. This study contributes to the understanding of the role of estrogen in the development of autoimmune arthritis and opens up new fields for research concerning the sex bias in autoimmune disease.

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