↓ Skip to main content

Michigan Publishing

Article Metrics

Photosensitivity and type I IFN responses in cutaneous lupus are driven by epidermal-derived interferon kappa

Overview of attention for article published in Annals of the Rheumatic Diseases, July 2018
Altmetric Badge

About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (95th percentile)
  • High Attention Score compared to outputs of the same age and source (94th percentile)

Mentioned by

news
5 news outlets
twitter
22 tweeters
facebook
1 Facebook page
googleplus
1 Google+ user

Citations

dimensions_citation
1 Dimensions

Readers on

mendeley
13 Mendeley
Title
Photosensitivity and type I IFN responses in cutaneous lupus are driven by epidermal-derived interferon kappa
Published in
Annals of the Rheumatic Diseases, July 2018
DOI 10.1136/annrheumdis-2018-213197
Pubmed ID
Authors

Mrinal K Sarkar, Grace A Hile, Lam C Tsoi, Xianying Xing, Jianhua Liu, Yun Liang, Celine C Berthier, William R Swindell, Matthew T Patrick, Shuai Shao, Pei-Suen Tsou, Ranjitha Uppala, Maria A Beamer, Anshika Srivastava, Stephanie L Bielas, Paul W Harms, Spiro Getsios, James T Elder, John J Voorhees, Johann E Gudjonsson, J Michelle Kahlenberg

Abstract

Skin inflammation and photosensitivity are common in patients with cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE), yet little is known about the mechanisms that regulate these traits. Here we investigate the role of interferon kappa (IFN-κ) in regulation of type I interferon (IFN) and photosensitive responses and examine its dysregulation in lupus skin. mRNA expression of type I IFN genes was analysed from microarray data of CLE lesions and healthy control skin. Similar expression in cultured primary keratinocytes, fibroblasts and endothelial cells was analysed via RNA-seq. IFNK knock-out (KO) keratinocytes were generated using CRISPR/Cas9. Keratinocytes stably overexpressing IFN-κ were created via G418 selection of transfected cells. IFN responses were assessed via phosphorylation of STAT1 and STAT2 and qRT-PCR for IFN-regulated genes. Ultraviolet B-mediated apoptosis was analysed via TUNEL staining. In vivo protein expression was assessed via immunofluorescent staining of normal and CLE lesional skin. IFNK is one of two type I IFNs significantly increased (1.5-fold change, false discovery rate (FDR) q<0.001) in lesional CLE skin. Gene ontology (GO) analysis showed that type I IFN responses were enriched (FDR=6.8×10-04) in keratinocytes not in fibroblast and endothelial cells, and this epithelial-derived IFN-κ is responsible for maintaining baseline type I IFN responses in healthy skin. Increased levels of IFN-κ, such as seen in SLE, amplify and accelerate responsiveness of epithelia to IFN-α and increase keratinocyte sensitivity to UV irradiation. Notably, KO of IFN-κ or inhibition of IFN signalling with baricitinib abrogates UVB-induced apoptosis. Collectively, our data identify IFN-κ as a critical IFN in CLE pathology via promotion of enhanced IFN responses and photosensitivity. IFN-κ is a potential novel target for UVB prophylaxis and CLE-directed therapy.

Twitter Demographics

The data shown below were collected from the profiles of 22 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 13 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 13 100%

Demographic breakdown

Readers by professional status Count As %
Other 3 23%
Student > Bachelor 2 15%
Student > Postgraduate 2 15%
Researcher 2 15%
Student > Ph. D. Student 2 15%
Other 2 15%
Readers by discipline Count As %
Medicine and Dentistry 5 38%
Immunology and Microbiology 3 23%
Agricultural and Biological Sciences 2 15%
Unspecified 2 15%
Biochemistry, Genetics and Molecular Biology 1 8%
Other 0 0%

Attention Score in Context

This research output has an Altmetric Attention Score of 55. 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 25 August 2018.
All research outputs
#250,949
of 12,063,292 outputs
Outputs from Annals of the Rheumatic Diseases
#86
of 4,723 outputs
Outputs of similar age
#11,503
of 247,183 outputs
Outputs of similar age from Annals of the Rheumatic Diseases
#3
of 55 outputs
Altmetric has tracked 12,063,292 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 97th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 4,723 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.3. This one has done particularly well, scoring higher than 98% 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 247,183 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 95% of its contemporaries.
We're also able to compare this research output to 55 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 94% of its contemporaries.