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Role of HLA-G and extracellular vesicles in renal cancer stem cell-induced inhibition of dendritic cell differentiation

Overview of attention for article published in BMC Cancer, December 2015
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (62nd percentile)
  • High Attention Score compared to outputs of the same age and source (82nd percentile)

Mentioned by

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5 tweeters

Citations

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32 Dimensions

Readers on

mendeley
29 Mendeley
Title
Role of HLA-G and extracellular vesicles in renal cancer stem cell-induced inhibition of dendritic cell differentiation
Published in
BMC Cancer, December 2015
DOI 10.1186/s12885-015-2025-z
Pubmed ID
Authors

Cristina Grange, Marta Tapparo, Stefania Tritta, Maria Chiara Deregibus, Antonino Battaglia, Paolo Gontero, Bruno Frea, Giovanni Camussi

Abstract

Tumor immune-escape has been related to the ability of cancer cells to inhibit T cell activation and dendritic cell (DC) differentiation. We previously identified a tumor initiating population, expressing the mesenchymal marker CD105, which fulfills the criteria for definition as cancer stem cells (CD105(+) CSCs) able to release extracellular vesicles (EVs) that favor tumor progression and metastases. The aim of the present study was to compare the ability of renal CSCs and derived EVs to modulate the behavior of monocyte-derived DCs with a non-tumor initiating renal cancer cell population (CD105(-) TCs) and their EVs. Maturation of monocyte-derived DCs was studied in presence of CD105(+) CSCs and CD105(-) TCs and their derived EVs. DC differentiation experiments were evaluated by cytofluorimetric analysis. T cell proliferation and ELISA assays were performed. Monocytes and T cells were purified from peripheral blood mononuclear cells obtained from healthy donors. The results obtained demonstrate that both CD105(+) CSCs and CD105(-) TCs impaired the differentiation process of DCs from monocytes. However, the immune-modulatory effect of CD105(+) CSCs was significantly greater than that of CD105(-) TCs. EVs derived from CD105(+) CSCs and in less extent, those derived from CD105(-) TCs retained the ability to impair monocyte maturation and T cell activation. The mechanism has been mainly related to the expression of HLA-G by tumor cells and to its release in a form associated to EVs. HLA-G blockade significantly reduced the inhibitory effect of EVs on DC differentiation. In conclusion, the results of the present study indicate that renal cancer cells and in particular CSCs and derived EVs impair maturation of DCs and T cell immune response by a mechanism involving HLA-G.

Twitter Demographics

The data shown below were collected from the profiles of 5 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 29 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 3%
Unknown 28 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 24%
Student > Master 5 17%
Researcher 4 14%
Student > Doctoral Student 3 10%
Unspecified 1 3%
Other 3 10%
Unknown 6 21%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 21%
Agricultural and Biological Sciences 6 21%
Medicine and Dentistry 3 10%
Immunology and Microbiology 2 7%
Unspecified 1 3%
Other 4 14%
Unknown 7 24%

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 15 May 2016.
All research outputs
#5,887,823
of 11,236,222 outputs
Outputs from BMC Cancer
#1,309
of 4,151 outputs
Outputs of similar age
#117,861
of 324,913 outputs
Outputs of similar age from BMC Cancer
#41
of 243 outputs
Altmetric has tracked 11,236,222 research outputs across all sources so far. This one is in the 47th percentile – i.e., 47% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,151 research outputs from this source. They receive a mean Attention Score of 3.9. This one has gotten more attention than average, scoring higher than 67% 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 324,913 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 62% of its contemporaries.
We're also able to compare this research output to 243 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 82% of its contemporaries.