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Cbl-b Deficiency in Mice Results in Exacerbation of Acute and Chronic Stages of Allergic Asthma

Overview of attention for article published in Frontiers in immunology, November 2015
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Title
Cbl-b Deficiency in Mice Results in Exacerbation of Acute and Chronic Stages of Allergic Asthma
Published in
Frontiers in immunology, November 2015
DOI 10.3389/fimmu.2015.00592
Pubmed ID
Authors

William F. Carson, Linda A. Guernsey, Anurag Singh, Eric R. Secor, Elizabeth A. Wohlfert, Robert B. Clark, Craig M. Schramm, Steven L. Kunkel, Roger S. Thrall

Abstract

Mice sensitized to ovalbumin (OVA) develop allergic airway disease (AAD) with short-term daily OVA aerosol challenge; inflammation resolves with long-term OVA aerosol exposure, resulting in local inhalational tolerance (LIT). Cbl-b is an E3 ubiquitin ligase involved with CD28 signaling; Cbl-b(-/-) effector T cells are resistant to regulatory T cell-mediated suppression in vitro and in vivo. The present study utilized Cbl-b(-/-) mice to investigate the role of Cbl-b in the development of AAD and LIT. Cbl-b(-/-) mice exhibited increased airway inflammation during AAD, which failed to resolve with long-term OVA aerosol exposure. Exacerbation of inflammation in Cbl-b(-/-) mice correlated with increased proinflammatory cytokine levels and expansion of effector T cells in the BAL during AAD, but did not result in either a modulation of lymphocyte subsets in systemic tissues or in OVA-specific IgE in serum. These results implicate a role for Cbl-b in the resolution of allergic airway inflammation.

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

Geographical breakdown

Country Count As %
Unknown 14 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 3 21%
Student > Postgraduate 2 14%
Researcher 2 14%
Student > Ph. D. Student 1 7%
Librarian 1 7%
Other 2 14%
Unknown 3 21%
Readers by discipline Count As %
Medicine and Dentistry 3 21%
Immunology and Microbiology 2 14%
Agricultural and Biological Sciences 1 7%
Computer Science 1 7%
Economics, Econometrics and Finance 1 7%
Other 3 21%
Unknown 3 21%
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 05 December 2015.
All research outputs
#16,047,334
of 25,373,627 outputs
Outputs from Frontiers in immunology
#16,703
of 31,516 outputs
Outputs of similar age
#213,935
of 392,711 outputs
Outputs of similar age from Frontiers in immunology
#77
of 135 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 31,516 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one is in the 42nd percentile – i.e., 42% 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 392,711 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 43rd percentile – i.e., 43% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 135 others from the same source and published within six weeks on either side of this one. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.