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Active immunization with myelin-derived altered peptide ligand reduces mechanical pain hypersensitivity following peripheral nerve injury

Overview of attention for article published in Journal of Neuroinflammation, February 2015
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Title
Active immunization with myelin-derived altered peptide ligand reduces mechanical pain hypersensitivity following peripheral nerve injury
Published in
Journal of Neuroinflammation, February 2015
DOI 10.1186/s12974-015-0253-4
Pubmed ID
Authors

Chamini J Perera, Samuel S Duffy, Justin G Lees, Cristina F Kim, Barbara Cameron, Vasso Apostolopoulos, Gila Moalem-Taylor

Abstract

T cells have been implicated in neuropathic pain that is caused by peripheral nerve injury. Immunogenic myelin basic protein (MBP) peptides have been shown to initiate mechanical allodynia in a T cell-dependent manner. Antagonistic altered peptide ligands (APLs) are peptides with substitutions in amino acid residues at T cell receptor contact sites and can inhibit T cell function and modulate inflammatory responses. In the present study, we studied the effects of immunization with MBP-derived APL on pain behavior and neuroinflammation in an animal model of peripheral nerve injury. Lewis rats were immunized subcutaneously at the base of the tail with either a weakly encephalitogenic peptide of MBP (cyclo-MBP87-99) or APL (cyclo-(87-99)[A(91),A(96)]MBP87-99) in complete Freund's adjuvant (CFA) or CFA only (control), following chronic constriction injury (CCI) of the left sciatic nerve. Pain hypersensitivity was tested by measurements of paw withdrawal threshold to mechanical stimuli, regulatory T cells in spleen and lymph nodes were analyzed by flow cytometry, and immune cell infiltration into the nervous system was assessed by immunohistochemistry (days 10 and 30 post-CCI). Cytokines were measured in serum and nervous tissue of nerve-injured rats (day 10 post-CCI). Rats immunized with the APL cyclo-(87-99)[A(91),A(96)]MBP87-99 had significantly reduced mechanical pain hypersensitivity in the ipsilateral hindpaw compared to cyclo-MBP87-99-treated and control rats. This was associated with significantly decreased infiltration of T cells and ED1+ macrophages in the injured nerve of APL-treated animals. The percentage of anti-inflammatory (M2) macrophages was significantly upregulated in the APL-treated rats on day 30 post-CCI. Compared to the control rats, microglial activation in the ipsilateral lumbar spinal cord was significantly increased in the MBP-treated rats, but was not altered in the rats immunized with the MBP-derived APL. In addition, immunization with the APL significantly increased splenic regulatory T cells. Several cytokines were significantly altered after CCI, but no significant difference was observed between the APL-treated and control rats. These results suggest that immune deviation by active immunization with a non-encephalitogenic MBP-derived APL mediates an analgesic effect in animals with peripheral nerve injury. Thus, T cell immunomodulation warrants further investigation as a possible therapeutic strategy for the treatment of peripheral neuropathic pain.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 47 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 2%
Unknown 46 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 13%
Student > Postgraduate 6 13%
Student > Master 6 13%
Student > Bachelor 5 11%
Student > Doctoral Student 4 9%
Other 10 21%
Unknown 10 21%
Readers by discipline Count As %
Neuroscience 7 15%
Biochemistry, Genetics and Molecular Biology 5 11%
Agricultural and Biological Sciences 5 11%
Nursing and Health Professions 4 9%
Veterinary Science and Veterinary Medicine 4 9%
Other 10 21%
Unknown 12 26%
Attention Score in Context

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 20 February 2015.
All research outputs
#21,320,623
of 26,184,649 outputs
Outputs from Journal of Neuroinflammation
#2,434
of 3,019 outputs
Outputs of similar age
#279,191
of 372,116 outputs
Outputs of similar age from Journal of Neuroinflammation
#36
of 47 outputs
Altmetric has tracked 26,184,649 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,019 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.0. This one is in the 11th percentile – i.e., 11% 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 372,116 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 47 others from the same source and published within six weeks on either side of this one. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.