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Recombinant human PDCD5 (rhPDCD5) protein is protective in a mouse model of multiple sclerosis

Overview of attention for article published in Journal of Neuroinflammation, June 2015
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Title
Recombinant human PDCD5 (rhPDCD5) protein is protective in a mouse model of multiple sclerosis
Published in
Journal of Neuroinflammation, June 2015
DOI 10.1186/s12974-015-0338-0
Pubmed ID
Authors

Juan Xiao, Wenwei Liu, Yingyu Chen, Wenbin Deng

Abstract

In multiple sclerosis (MS) and its widely used animal model, experimental autoimmune encephalomyelitis (EAE), autoreactive T cells contribute importantly to central nervous system (CNS) tissue damage and disease progression. Promoting apoptosis of autoreactive T cells may help eliminate cells responsible for inflammation and may delay disease progression and decrease the frequency and severity of relapse. Programmed cell death 5 (PDCD5) is a protein known to accelerate apoptosis in response to various stimuli. However, the effects of recombinant human PDCD5 (rhPDCD5) on encephalitogenic T cell-mediated inflammation remain unknown. We examined the effects of intraperitoneal injection of rhPDCD5 (10 mg/kg) on EAE both prophylactically (started on day 0 post-EAE induction) and therapeutically (started on the onset of EAE disease at day 8), with both of the treatment paradigms being given every other day until day 25. Repeated measures two-way analysis of variance was used for statistical analysis. We showed that the anti-inflammatory effects of rhPDCD5 were due to a decrease in Th1/Th17 cell frequency, accompanied by a reduction of proinflammatory cytokines, including IFN-γ and IL-17A, and were observed in both prophylactic and therapeutic regimens of rhPDCD5 treatment in EAE mice. Moreover, rhPDCD5-induced apoptosis of myelin-reactive CD4(+) T cells, along with the upregulation of Bax and downregulation of Bcl-2, and with activated caspase 3. Our data demonstrate that rhPDCD5 ameliorates the autoimmune CNS disease by inhibiting Th1/Th17 differentiation and inducing apoptosis of predominantly pathogenic T cells. This study provides a novel mechanism to explain the effects of rhPDCD5 on neural inflammation. The work represents a translational demonstration that rhPDCD5 has prophylactic and therapeutic properties in a model of multiple sclerosis.

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The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 26 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 4%
Unknown 25 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 19%
Student > Master 5 19%
Student > Doctoral Student 3 12%
Other 3 12%
Student > Bachelor 2 8%
Other 7 27%
Unknown 1 4%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 15%
Medicine and Dentistry 4 15%
Agricultural and Biological Sciences 4 15%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Immunology and Microbiology 2 8%
Other 8 31%
Unknown 2 8%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 24 March 2016.
All research outputs
#14,228,602
of 22,811,321 outputs
Outputs from Journal of Neuroinflammation
#1,562
of 2,629 outputs
Outputs of similar age
#136,759
of 264,930 outputs
Outputs of similar age from Journal of Neuroinflammation
#27
of 49 outputs
Altmetric has tracked 22,811,321 research outputs across all sources so far. This one is in the 35th percentile – i.e., 35% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,629 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. 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 264,930 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 49 others from the same source and published within six weeks on either side of this one. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.