You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output.
Click here to find out more.
X Demographics
Mendeley readers
Attention Score in Context
| Title |
Tissue specific CD4+ T cell priming determines the requirement for interleukin-23 in experimental arthritis
|
|---|---|
| Published in |
Arthritis Research & Therapy, September 2014
|
| DOI | 10.1186/s13075-014-0440-1 |
| Pubmed ID | |
| Authors |
Susan A Olalekan, Yanxia Cao, Alison Finnegan |
| Abstract |
IntroductionRheumatoid arthritis (RA) is a chronic inflammatory disease with striking heterogeneity in (i) clinical presentation, (ii) autoantibody profiles and (iii) responses to treatment suggesting that distinct molecular mechanisms may underlie the disease process. Proteoglycan-induced arthritis (PGIA) is induced by two pathways either by intraperitoneal (i.p.) or subcutaneous (s.c.) exposure to PG. CD4+ T cells primed by the i.p. route are T helper (Th)1 cells expressing interferon gamma (IFN-¿) whereas CD4+ T cells primed by the s.c. route are Th17 cells expressing interleukin (IL)-17. IL-23 is necessary for maintaining the phenotype of Th17 cells; however, IL-23 is inflammatory independent of IL-17. The aim of this study was to determine if PGIA induced by different routes of immunization is dependent on IL-23.MethodsBALB/c wild type (WT), IL-12p40¿/¿ and IL-23p19¿/¿ littermate mice were immunized with recombinant G1 (rG1) domain of human PG in adjuvant either i.p. or s.c. and development of arthritis monitored. Joint histology was assessed. CD4+ T cell cytokines in spleen, lymph node (LN), and joint were assessed by intracellular staining and cytokine enzyme-linked immunosorbent assay. RNA transcripts for cytokines and transcription factors were examined.ResultsPGIA was suppressed in the p40¿/¿ and p19¿/¿ mice immunized by the s.c. route but only inhibited in p40¿/¿ mice by the i.p. route. The joints of s.c. but not i.p. sensitized mice contained a population of CD4+ T cells expressing single positive IFN-¿ and IL-17 and double positive IFN-¿/IL-17 which were dependent on IL-23 expression. The IFN-¿ and IL-17 response in spleen and inguinal LN was inhibited in p19¿/¿ mice and p40¿/¿ mice after s.c. immunization, whereas in i.p. immunized p19¿/¿ mice, IL-17 but not IFN-¿ was reduced. Inguinal LN CD11c+ dendritic cells (DC) from s.c. immunized, but not spleen DC from i.p. immunized mice, produced IL-23, IL-1ß, and IL-6 and activated T cells to produce IL-17.ConclusionIL-23 is necessary for the activity of Th17 after s.c. immunization and does not play a role independent of IL-17 after i.p. immunization. These data demonstrate that the molecular pathways IL-23/17 and IL-12/IFN-¿ may represent subtypes of arthritis determined by the mode of induction. |
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 15 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 15 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Doctoral Student | 3 | 20% |
| Student > Ph. D. Student | 3 | 20% |
| Student > Bachelor | 2 | 13% |
| Student > Master | 2 | 13% |
| Researcher | 2 | 13% |
| Other | 2 | 13% |
| Unknown | 1 | 7% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 5 | 33% |
| Medicine and Dentistry | 5 | 33% |
| Immunology and Microbiology | 2 | 13% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 13% |
| Unknown | 1 | 7% |
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 27 September 2014.
All research outputs
#17,286,645
of 25,374,917 outputs
Outputs from Arthritis Research & Therapy
#2,536
of 3,381 outputs
Outputs of similar age
#157,699
of 263,060 outputs
Outputs of similar age from Arthritis Research & Therapy
#33
of 49 outputs
Altmetric has tracked 25,374,917 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,381 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.2. This one is in the 16th percentile – i.e., 16% 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 263,060 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 49 others from the same source and published within six weeks on either side of this one. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.