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Aquaporin 4-specific T cells and NMO-IgG cause primary retinal damage in experimental NMO/SD

Overview of attention for article published in Acta Neuropathologica Communications, August 2016
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Title
Aquaporin 4-specific T cells and NMO-IgG cause primary retinal damage in experimental NMO/SD
Published in
Acta Neuropathologica Communications, August 2016
DOI 10.1186/s40478-016-0355-y
Pubmed ID
Authors

Bleranda Zeka, Maria Hastermann, Nathalie Kaufmann, Kathrin Schanda, Marko Pende, Tatsuro Misu, Paulus Rommer, Kazuo Fujihara, Ichiro Nakashima, Charlotte Dahle, Fritz Leutmezer, Markus Reindl, Hans Lassmann, Monika Bradl

Abstract

Neuromyelitis optica/spectrum disorder (NMO/SD) is a severe, inflammatory disease of the central nervous system (CNS). In the majority of patients, it is associated with the presence of pathogenic serum autoantibodies (the so-called NMO-IgGs) directed against the water channel aquaporin 4 (AQP4), and with the formation of large, astrocyte-destructive lesions in spinal cord and optic nerves. A large number of recent studies using optical coherence tomography (OCT) demonstrated that damage to optic nerves in NMO/SD is also associated with retinal injury, as evidenced by retinal nerve fiber layer (RNFL) thinning and microcystic inner nuclear layer abnormalities. These studies concluded that retinal injury in NMO/SD patients results from secondary neurodegeneration triggered by optic neuritis.However, the eye also contains cells expressing AQP4, i.e., Müller cells and astrocytes in the retina, epithelial cells of the ciliary body, and epithelial cells of the iris, which raised the question whether the eye can also be a primary target in NMO/SD. Here, we addressed this point in experimental NMO/SD (ENMO) induced in Lewis rat by transfer of AQP4268-285-specific T cells and NMO-IgG.We show that these animals show retinitis and subsequent dysfunction/damage of retinal axons and neurons, and that this pathology occurs independently of the action of NMO-IgG. We further show that in the retinae of ENMO animals Müller cell side branches lose AQP4 reactivity, while retinal astrocytes and Müller cell processes in the RNFL/ganglionic cell layers are spared. These changes only occur in the presence of both AQP4268-285-specific T cells and NMO-IgG.Cumulatively, our data show that damage to retinal cells can be a primary event in NMO/SD.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 62 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 62 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 11 18%
Student > Master 11 18%
Student > Ph. D. Student 7 11%
Student > Doctoral Student 6 10%
Student > Postgraduate 5 8%
Other 12 19%
Unknown 10 16%
Readers by discipline Count As %
Medicine and Dentistry 17 27%
Neuroscience 15 24%
Biochemistry, Genetics and Molecular Biology 6 10%
Immunology and Microbiology 5 8%
Agricultural and Biological Sciences 4 6%
Other 1 2%
Unknown 14 23%
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 28 August 2016.
All research outputs
#14,269,286
of 22,882,389 outputs
Outputs from Acta Neuropathologica Communications
#1,077
of 1,382 outputs
Outputs of similar age
#213,995
of 364,241 outputs
Outputs of similar age from Acta Neuropathologica Communications
#22
of 35 outputs
Altmetric has tracked 22,882,389 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 1,382 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 12.8. This one is in the 19th percentile – i.e., 19% 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 364,241 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 35 others from the same source and published within six weeks on either side of this one. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.