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Absence of system xc − on immune cells invading the central nervous system alleviates experimental autoimmune encephalitis

Overview of attention for article published in Journal of Neuroinflammation, January 2017
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Title
Absence of system xc − on immune cells invading the central nervous system alleviates experimental autoimmune encephalitis
Published in
Journal of Neuroinflammation, January 2017
DOI 10.1186/s12974-016-0787-0
Pubmed ID
Authors

Ellen Merckx, Giulia Albertini, Magdalena Paterka, Cathy Jensen, Philipp Albrecht, Michael Dietrich, Joeri Van Liefferinge, Eduard Bentea, Lise Verbruggen, Thomas Demuyser, Lauren Deneyer, Jan Lewerenz, Geert van Loo, Jacques De Keyser, Hideyo Sato, Pamela Maher, Axel Methner, Ann Massie

Abstract

Multiple sclerosis (MS) is an autoimmune demyelinating disease that affects the central nervous system (CNS), leading to neurodegeneration and chronic disability. Accumulating evidence points to a key role for neuroinflammation, oxidative stress, and excitotoxicity in this degenerative process. System xc(-) or the cystine/glutamate antiporter could tie these pathological mechanisms together: its activity is enhanced by reactive oxygen species and inflammatory stimuli, and its enhancement might lead to the release of toxic amounts of glutamate, thereby triggering excitotoxicity and neurodegeneration. Semi-quantitative Western blotting served to study protein expression of xCT, the specific subunit of system xc(-), as well as of regulators of xCT transcription, in the normal appearing white matter (NAWM) of MS patients and in the CNS and spleen of mice exposed to experimental autoimmune encephalomyelitis (EAE), an accepted mouse model of MS. We next compared the clinical course of the EAE disease, the extent of demyelination, the infiltration of immune cells and microglial activation in xCT-knockout (xCT(-/-)) mice and irradiated mice reconstituted in xCT(-/-) bone marrow (BM), to their proper wild type (xCT(+/+)) controls. xCT protein expression levels were upregulated in the NAWM of MS patients and in the brain, spinal cord, and spleen of EAE mice. The pathways involved in this upregulation in NAWM of MS patients remain unresolved. Compared to xCT(+/+) mice, xCT(-/-) mice were equally susceptible to EAE, whereas mice transplanted with xCT(-/-) BM, and as such only exhibiting loss of xCT in their immune cells, were less susceptible to EAE. In none of the above-described conditions, demyelination, microglial activation, or infiltration of immune cells were affected. Our findings demonstrate enhancement of xCT protein expression in MS pathology and suggest that system xc(-) on immune cells invading the CNS participates to EAE. Since a total loss of system xc(-) had no net beneficial effects, these results have important implications for targeting system xc(-) for treatment of MS.

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 64 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 64 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 13 20%
Student > Bachelor 12 19%
Student > Master 11 17%
Student > Ph. D. Student 6 9%
Student > Doctoral Student 2 3%
Other 2 3%
Unknown 18 28%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 10 16%
Neuroscience 10 16%
Nursing and Health Professions 8 13%
Medicine and Dentistry 5 8%
Pharmacology, Toxicology and Pharmaceutical Science 3 5%
Other 6 9%
Unknown 22 34%

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 06 October 2017.
All research outputs
#9,111,809
of 11,877,834 outputs
Outputs from Journal of Neuroinflammation
#898
of 1,357 outputs
Outputs of similar age
#215,050
of 327,956 outputs
Outputs of similar age from Journal of Neuroinflammation
#17
of 27 outputs
Altmetric has tracked 11,877,834 research outputs across all sources so far. This one is in the 20th percentile – i.e., 20% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,357 research outputs from this source. They receive a mean Attention Score of 4.9. This one is in the 28th percentile – i.e., 28% 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 327,956 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 29th percentile – i.e., 29% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 27 others from the same source and published within six weeks on either side of this one. This one is in the 29th percentile – i.e., 29% of its contemporaries scored the same or lower than it.