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

Overview of attention for article published in Arthritis Research & Therapy, January 2015
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Title
Estrogen regulates T helper 17 phenotype and localization in experimental autoimmune arthritis
Published in
Arthritis Research & Therapy, January 2015
DOI 10.1186/s13075-015-0548-y
Pubmed ID
Authors

Annica Andersson, Alexandra Stubelius, Merja Karlsson, Cecilia Engdahl, Malin Erlandsson, Louise Grahnemo, Marie K Lagerquist, Ulrika Islander

Abstract

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. Ovariectomized DBA/1 mice treated with 17β-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 α-knockout mice (ERα(-/-)) and wild-type littermates, treated with E2 or placebo and subjected to antigen-induced arthritis. 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 ERα. 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. 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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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 57 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
India 1 2%
Brazil 1 2%
Unknown 55 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 14 25%
Student > Bachelor 9 16%
Researcher 8 14%
Student > Doctoral Student 4 7%
Student > Master 4 7%
Other 8 14%
Unknown 10 18%
Readers by discipline Count As %
Medicine and Dentistry 13 23%
Agricultural and Biological Sciences 11 19%
Biochemistry, Genetics and Molecular Biology 8 14%
Immunology and Microbiology 4 7%
Nursing and Health Professions 2 4%
Other 6 11%
Unknown 13 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 April 2015.
All research outputs
#13,198,118
of 22,797,621 outputs
Outputs from Arthritis Research & Therapy
#1,836
of 2,977 outputs
Outputs of similar age
#168,800
of 353,063 outputs
Outputs of similar age from Arthritis Research & Therapy
#36
of 56 outputs
Altmetric has tracked 22,797,621 research outputs across all sources so far. This one is in the 41st percentile – i.e., 41% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,977 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.9. This one is in the 37th percentile – i.e., 37% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 353,063 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 51% of its contemporaries.
We're also able to compare this research output to 56 others from the same source and published within six weeks on either side of this one. This one is in the 35th percentile – i.e., 35% of its contemporaries scored the same or lower than it.