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JAK3-STAT pathway blocking benefits in experimental lupus nephritis

Overview of attention for article published in Arthritis Research & Therapy, June 2016
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Title
JAK3-STAT pathway blocking benefits in experimental lupus nephritis
Published in
Arthritis Research & Therapy, June 2016
DOI 10.1186/s13075-016-1034-x
Pubmed ID
Authors

Èlia Ripoll, Laura de Ramon, Juliana Draibe, Ana Merino, Nuria Bolaños, Montse Goma, Josep M. Cruzado, Josep M. Grinyó, Juan Torras

Abstract

Lupus nephritis (LN) is a complex chronic autoimmune disease of unknown etiology characterized by loss of tolerance against several self-antigens. Cytokines are known to be central players in LN pathogenesis. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is one important pathway that mediates signal transduction of several cytokines. In this study, we examined the pathogenic role of this pathway and how CP-690,550 treatment influences LN outcome. Six-month-old NZB/NZWF1 mice were divided into two different treatment groups: (1) control animals given vehicle treatment, cyclophosphamide, and mycophenolate mofetil treatment as positive controls of the therapy and (2) mice treated with CP-690,550, a JAK3 inhibitor. Mice were treated for 12 weeks. We evaluated renal function, anti-double-stranded DNA (anti-dsDNA) antibody, renal histology changes, kidney complement and immunoglobulin G (IgG) deposits, T-cell and macrophage infiltration, kidney inflammatory gene expression, and circulating cytokine changes. CP-690,550 treatment significantly reduced proteinuria and improved renal function and histological lesions of the kidney. Compared with vehicle-treated animals, those undergoing CP-690,550 treatment showed significantly diminished anti-dsDNA antibody and complement component C3 and IgG deposition in glomeruli. We also observed a significant reduction of T-cell and macrophage infiltration. Kidney gene expression revealed a reduction in inflammatory cytokines and complement and related macrophage-attracting genes. Circulating inflammatory cytokines were also reduced with treatment. On the basis of our results, we conclude that the JAK-STAT pathway is implicated in the progression of renal inflammation in NZB/WF1 mice and that targeting JAK3 with CP-690,550 is effective in slowing down the course of experimental LN. Thus, CP-690,550 could become a new therapeutic tool in LN and other autoimmune diseases.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 34 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 34 100%

Demographic breakdown

Readers by professional status Count As %
Other 6 18%
Student > Ph. D. Student 6 18%
Student > Master 5 15%
Researcher 4 12%
Student > Bachelor 3 9%
Other 5 15%
Unknown 5 15%
Readers by discipline Count As %
Medicine and Dentistry 10 29%
Biochemistry, Genetics and Molecular Biology 5 15%
Immunology and Microbiology 4 12%
Agricultural and Biological Sciences 3 9%
Veterinary Science and Veterinary Medicine 2 6%
Other 5 15%
Unknown 5 15%

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 15 June 2017.
All research outputs
#8,931,411
of 11,622,318 outputs
Outputs from Arthritis Research & Therapy
#1,318
of 1,602 outputs
Outputs of similar age
#177,453
of 269,757 outputs
Outputs of similar age from Arthritis Research & Therapy
#15
of 23 outputs
Altmetric has tracked 11,622,318 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 1,602 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.5. This one is in the 17th percentile – i.e., 17% of its peers scored the same or lower than it.
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We're also able to compare this research output to 23 others from the same source and published within six weeks on either side of this one. This one is in the 17th percentile – i.e., 17% of its contemporaries scored the same or lower than it.