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Phosphatase and tensin homolog (PTEN) in antigen-presenting cells controls Th17-mediated autoimmune arthritis

Overview of attention for article published in Arthritis Research & Therapy, August 2015
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Title
Phosphatase and tensin homolog (PTEN) in antigen-presenting cells controls Th17-mediated autoimmune arthritis
Published in
Arthritis Research & Therapy, August 2015
DOI 10.1186/s13075-015-0742-y
Pubmed ID
Authors

Stephan Blüml, Emine Sahin, Victoria Saferding, Eliana Goncalves-Alves, Eva Hainzl, Birgit Niederreiter, Anastasia Hladik, Tobias Lohmeyer, Julia S. Brunner, Michael Bonelli, Marije I. Koenders, Wim B. van den Berg, Giulio Superti-Furga, Josef S. Smolen, Gernot Schabbauer, Kurt Redlich

Abstract

Autoreactive T cells are a central element in many systemic autoimmune diseases. The generation of these pathogenic T cells is instructed by antigen-presenting cells (APCs). However, signaling pathways in APCs that drive autoimmune diseases, such as rheumatoid arthritis, are not understood. We measured phenotypic maturation, cytokine production and induction of T cell proliferation of APCs derived from wt mice and mice with a myeloid-specific deletion of PTEN (myeloid PTEN(-/-)) in vitro and in vivo. We induced collagen-induced arthritis (CIA) and K/BxN serum transfer arthritis in wt and myeloid-specific PTEN(-/-) mice. We measured the cellular composition of lymph nodes by flow cytometry and cytokines in serum and after ex vivo stimulation of T cells. We show that myeloid-specific PTEN(-/-) mice are almost protected from CIA. Myeloid-specific deletion of PTEN leads to a significant reduction of cytokine expression pivotal for the induction of systemic autoimmunity such as interleukin (IL)-23 and IL-6, leading to a significant reduction of a Th17 type of immune response characterized by reduced production of IL-17 and IL-22. In contrast, myeloid-specific PTEN deficiency did not affect K/BxN serum transfer arthritis, which is independent of the adaptive immune system and solely depends on innate effector functions. These data demonstrate that the presence of PTEN in myeloid cells is required for the development of CIA. Deletion of PTEN in myeloid cells inhibits the development of autoimmune arthritis by preventing the generation of a pathogenic Th17 type of immune response.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 30%
Researcher 4 20%
Student > Bachelor 2 10%
Student > Postgraduate 2 10%
Student > Doctoral Student 1 5%
Other 1 5%
Unknown 4 20%
Readers by discipline Count As %
Immunology and Microbiology 4 20%
Medicine and Dentistry 4 20%
Agricultural and Biological Sciences 3 15%
Biochemistry, Genetics and Molecular Biology 3 15%
Psychology 1 5%
Other 1 5%
Unknown 4 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 21 May 2016.
All research outputs
#9,968,371
of 12,451,992 outputs
Outputs from Arthritis Research & Therapy
#1,716
of 1,983 outputs
Outputs of similar age
#186,286
of 267,400 outputs
Outputs of similar age from Arthritis Research & Therapy
#1
of 2 outputs
Altmetric has tracked 12,451,992 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
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