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IL-15 enhances the antitumor effect of human antigen-specific CD8+ T cells by cellular senescence delay

Overview of attention for article published in OncoImmunology, October 2016
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Title
IL-15 enhances the antitumor effect of human antigen-specific CD8+ T cells by cellular senescence delay
Published in
OncoImmunology, October 2016
DOI 10.1080/2162402x.2016.1237327
Pubmed ID
Authors

Jinsheng Weng, Kelsey E. Moriarty, Flavio Egidio Baio, Fuliang Chu, Sung-Doo Kim, Jin He, Zuliang Jie, Xiaoping Xie, Wencai Ma, Jianfei Qian, Liang Zhang, Jing Yang, Qing Yi, Sattva S. Neelapu, Larry W. Kwak

Abstract

Optimal expansion protocols for adoptive human T-cell therapy often include interleukin (IL)-15; however, the mechanism by which IL-15 improves the in vivo antitumor effect of T cells remains to be elucidated. Using human T cells generated from HLA-A2+ donors against novel T-cell epitopes derived from the human U266 myeloma cell line Ig light chain V-region (idiotype) as a model, we found that T cells cultured with IL-15 provided superior resistance to tumor growth in vivo, compared with IL-2, after adoptive transfer into immunodeficient hosts. This effect of IL-15 was associated with delayed/reversed senescence in tumor antigen-specific memory CD8(+) T cells mediated through downregulation of P21(WAF1), P16(INK4a), and P53 expression. Compared to IL-2, IL-15 stimulation dramatically activated JAK3-STAT5 signaling and inhibited the expression of DNA damage genes. Thus, our study elucidates a new mechanism for IL-15 in the regulation of STAT signaling pathways and CD8(+) T-cell senescence.

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The data shown below were collected from the profiles of 6 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 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 26%
Researcher 5 19%
Student > Doctoral Student 3 11%
Student > Bachelor 2 7%
Other 2 7%
Other 2 7%
Unknown 6 22%
Readers by discipline Count As %
Immunology and Microbiology 8 30%
Biochemistry, Genetics and Molecular Biology 5 19%
Medicine and Dentistry 4 15%
Agricultural and Biological Sciences 3 11%
Unknown 7 26%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 30 January 2017.
All research outputs
#8,672,743
of 25,703,943 outputs
Outputs from OncoImmunology
#850
of 2,183 outputs
Outputs of similar age
#121,236
of 328,786 outputs
Outputs of similar age from OncoImmunology
#25
of 39 outputs
Altmetric has tracked 25,703,943 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,183 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.5. This one has gotten more attention than average, scoring higher than 52% of its peers.
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 328,786 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 39 others from the same source and published within six weeks on either side of this one. This one is in the 25th percentile – i.e., 25% of its contemporaries scored the same or lower than it.