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Regulation of Foxp3+ Inducible Regulatory T Cell Stability by SOCS2

Overview of attention for article published in The Journal of Immunology, March 2013
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Title
Regulation of Foxp3+ Inducible Regulatory T Cell Stability by SOCS2
Published in
The Journal of Immunology, March 2013
DOI 10.4049/jimmunol.1201396
Pubmed ID
Authors

Camille A. Knosp, Chris Schiering, Shaun Spence, Helen P. Carroll, Hendrick J. Nel, Megan Osbourn, Ruaidhri Jackson, Oksana Lyubomska, Bernard Malissen, Rebecca Ingram, Denise C. Fitzgerald, Fiona Powrie, Padraic G. Fallon, James A. Johnston, Adrien Kissenpfennig, Knosp, C. A., Schiering, C., Spence, S., Carroll, H. P., Nel, H. J., Osbourn, M., Jackson, R., Lyubomska, O., Malissen, B., Ingram, R., Fitzgerald, D. C., Powrie, F., Fallon, P. G., Johnston, J. A., Kissenpfennig, A.

Abstract

Suppressor of cytokine signaling (SOCS) proteins are key regulators of CD4(+) T cell differentiation, and in particular, we have recently shown that SOCS2 inhibits the development of Th2 cells and allergic immune responses. Interestingly, transcriptome analyses have identified SOCS2 as being preferentially expressed in both natural regulatory T cells (Tregs) and inducible Tregs (iTregs); however, the role of SOCS2 in Foxp3(+) Treg function or development has not been fully elucidated. In this study, we show that despite having no effect on natural Treg development or function, SOCS2 is highly expressed in iTregs and required for the stable expression of Foxp3 in iTregs in vitro and in vivo. Indeed, SOCS2-deficient CD4(+) T cells upregulated Foxp3 following in vitro TGF-β stimulation, but failed to maintain stable expression of Foxp3. Moreover, in vivo generation of iTregs following OVA feeding was impaired in the absence of SOCS2 and could be rescued in the presence of IL-4 neutralizing Ab. Following IL-4 stimulation, SOCS2-deficient Foxp3(+) iTregs secreted elevated IFN-γ and IL-13 levels and displayed enhanced STAT6 phosphorylation. Therefore, we propose that SOCS2 regulates iTreg stability by downregulating IL-4 signaling. Moreover, SOCS2 is essential to maintain the anti-inflammatory phenotype of iTregs by preventing the secretion of proinflammatory cytokines. Collectively, these results suggest that SOCS2 may prevent IL-4-induced Foxp3(+) iTreg instability. Foxp3(+) iTregs are key regulators of immune responses at mucosal surfaces; therefore, this dual role of SOCS2 in both Th2 and Foxp3(+) iTregs reinforces SOCS2 as a potential therapeutic target for Th2-biased diseases.

Mendeley readers

The data shown below were compiled from readership statistics for 61 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 2%
France 1 2%
United States 1 2%
Korea, Republic of 1 2%
Sweden 1 2%
Unknown 56 92%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 20 33%
Researcher 19 31%
Student > Master 5 8%
Student > Doctoral Student 4 7%
Student > Bachelor 3 5%
Other 10 16%
Readers by discipline Count As %
Agricultural and Biological Sciences 36 59%
Medicine and Dentistry 7 11%
Biochemistry, Genetics and Molecular Biology 4 7%
Neuroscience 4 7%
Unspecified 3 5%
Other 7 11%

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 23 April 2013.
All research outputs
#4,196,599
of 7,992,147 outputs
Outputs from The Journal of Immunology
#3,792
of 6,871 outputs
Outputs of similar age
#57,189
of 118,304 outputs
Outputs of similar age from The Journal of Immunology
#31
of 78 outputs
Altmetric has tracked 7,992,147 research outputs across all sources so far. This one is in the 27th percentile – i.e., 27% of other outputs scored the same or lower than it.
So far Altmetric has tracked 6,871 research outputs from this source. They receive a mean Attention Score of 2.8. This one is in the 26th percentile – i.e., 26% 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 118,304 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 39th percentile – i.e., 39% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 78 others from the same source and published within six weeks on either side of this one. This one is in the 30th percentile – i.e., 30% of its contemporaries scored the same or lower than it.