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Control of B‐cell lymphoma by therapeutic vaccination and acquisition of immune resistance is independent of direct tumour IFN‐gamma signalling

Overview of attention for article published in Immunology & Cell Biology, February 2016
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Title
Control of B‐cell lymphoma by therapeutic vaccination and acquisition of immune resistance is independent of direct tumour IFN‐gamma signalling
Published in
Immunology & Cell Biology, February 2016
DOI 10.1038/icb.2016.9
Pubmed ID
Authors

Rory Rearden, Amelia Sah, Brianna Doff, Takumi Kobayashi, Sara J McKee, Graham R Leggatt, Stephen R Mattarollo

Abstract

Immunomodulatory therapies can effectively control haematological malignancies by promoting anti-tumour immunity. Previously we reported transient control growth of poorly immunogenic murine non-Hodgkin B cell lymphomas (B-NHL) by targeting natural killer T (NKT) cells with a therapeutic vaccine approach. Therapeutic efficacy was highly dependent on the ability of the vaccine to provoke rapid IFNγ production from NKT and NK cells. By manipulating the capacity of either host or lymphoma cells to signal through the IFNγ receptor (IFNγR) we investigated whether the therapeutic effect conferred by vaccine-induced IFNγ is a result of immune cell activation, lymphoma IFNγ sensitivity, or a combination of both. We demonstrated that anti-tumor immunity elicited by vaccination requires IFNγ-signalling within host cells, but not tumor cells. IFNγR deficient mice failed to mount an effective anti-tumor immune response following vaccination despite elevated IFNγ levels. With successive exposure to vaccination, lymphomas acquired an increasingly therapy-resistant phenotype and displayed a reduction in MHCI and CD1d surface expression, which is independent of tumor intrinsic IFNγ-signalling. Our results suggest that immunotherapy-induced IFNγ production mainly exerts its therapeutic effect via signalling through host cells, rather than directly to tumor cells in B-NHL. This signifies that intact IFNγ signalling within patients' immune compartment rather than tumor cell sensitivity to IFNγ is more critical for successful treatment. Finally, tumor IFNγ-signalling alone does not drive acquired tumor resistance to vaccination, implying that additional immunoediting pathways are responsible tumour immune escape.Immunology and Cell Biology accepted article preview online, 20 January 2016. doi:10.1038/icb.2016.9.

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X Demographics

The data shown below were collected from the profiles of 5 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 8 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 8 100%

Demographic breakdown

Readers by professional status Count As %
Other 2 25%
Student > Bachelor 1 13%
Student > Ph. D. Student 1 13%
Researcher 1 13%
Professor > Associate Professor 1 13%
Other 0 0%
Unknown 2 25%
Readers by discipline Count As %
Medicine and Dentistry 2 25%
Immunology and Microbiology 1 13%
Agricultural and Biological Sciences 1 13%
Neuroscience 1 13%
Chemistry 1 13%
Other 0 0%
Unknown 2 25%
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 May 2019.
All research outputs
#14,599,900
of 25,373,627 outputs
Outputs from Immunology & Cell Biology
#1,361
of 1,848 outputs
Outputs of similar age
#197,855
of 409,550 outputs
Outputs of similar age from Immunology & Cell Biology
#23
of 30 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 41st percentile – i.e., 41% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,848 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.3. This one is in the 24th percentile – i.e., 24% 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 409,550 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.
We're also able to compare this research output to 30 others from the same source and published within six weeks on either side of this one. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.