| Title |
Cause and consequences of the activated type I interferon system in SLE
|
|---|---|
| Published in |
Journal of Molecular Medicine, April 2016
|
| DOI | 10.1007/s00109-016-1421-4 |
| Pubmed ID | |
| Authors |
Maija-Leena Eloranta, Lars Rönnblom |
| Abstract |
Patients with systemic lupus erythematosus (SLE) have an increased expression of type I interferon (IFN)-regulated genes (an IFN signature), which is caused by an ongoing production of type I IFNs by plasmacytoid dendritic cells (pDCs). The reasons behind the continuous IFN production in SLE are the presence of self-derived IFN inducers and a lack of negative feed-back signals that downregulate the IFN response. In addition, several cells in the immune system promote the IFN production by pDCs and gene variants in the type I IFN signaling pathway contribute to the IFN signature. The type I IFNs act as an immune adjuvant and stimulate T cells, B cells, and monocytes, which all play an important role in the loss of tolerance and persistent autoimmune reaction in SLE. Consequently, new treatments aiming to inhibit the activated type I IFN system in SLE are now being developed and investigated in clinical trials. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United Kingdom | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 70 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 11 | 16% |
| Researcher | 9 | 13% |
| Student > Bachelor | 8 | 11% |
| Other | 6 | 9% |
| Student > Doctoral Student | 4 | 6% |
| Other | 7 | 10% |
| Unknown | 25 | 36% |
| Readers by discipline | Count | As % |
|---|---|---|
| Immunology and Microbiology | 12 | 17% |
| Medicine and Dentistry | 12 | 17% |
| Biochemistry, Genetics and Molecular Biology | 9 | 13% |
| Agricultural and Biological Sciences | 3 | 4% |
| Neuroscience | 2 | 3% |
| Other | 3 | 4% |
| Unknown | 29 | 41% |
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 22 April 2016.
All research outputs
#15,369,653
of 22,865,319 outputs
Outputs from Journal of Molecular Medicine
#1,135
of 1,551 outputs
Outputs of similar age
#179,622
of 299,364 outputs
Outputs of similar age from Journal of Molecular Medicine
#11
of 21 outputs
Altmetric has tracked 22,865,319 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,551 research outputs from this source. They receive a mean Attention Score of 5.0. This one is in the 21st percentile – i.e., 21% 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 299,364 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 31st percentile – i.e., 31% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 21 others from the same source and published within six weeks on either side of this one. This one is in the 33rd percentile – i.e., 33% of its contemporaries scored the same or lower than it.