Evidence map›Paper›PMID 26792955›Full record

ReviewMediators of inflammation2015

Targeting Th17 Cells with Small Molecules and Small Interference RNA.

Hui Lin, Pingfang Song, Yi Zhao, Li-Jia Xue, Yi Liu, Cong-Qiu Chu

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Aptamer-based applications for cardiovascular disease.Frontiers in bioengineering and biotechnology · 2022
    Review
  5. Review
  6. Article
  7. Applications of RNA interference in the treatment of arthritis.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
  8. Silencing RORγt in Human CD4Scientific reports · 2019
    Article
  9. Review
  10. Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Hui LinDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Pingfang SongDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University and VA Portland Health Care System, Portland, OR 97239, USA.
Yi ZhaoDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Li-Jia XueDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Yi LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Cong-Qiu ChuDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University and VA Portland Health Care System, Portland, OR 97239, USA.
Sichuan University · CNWest China Hospital of Sichuan University · CNOregon Health & Science University · USVA Portland Health Care System · US

Funding

Positive and Negative Regulation of IL-17 in Experimental ArthritisK08AR055254 · NIAMS · UNIVERSITY OF WASHINGTON · PI CHU, CONG-QIU · 2008 to 2011
$488k
NIAMS NIH HHS AR55254NIAMS NIH HHS K08 AR055254
6 · The paper itself

Abstract

T helper 17 (Th17) cells play a central role in inflammatory and autoimmune diseases via the production of proinflammatory cytokines interleukin- (IL-) 17, IL-17F, and IL-22. Anti-IL-17 monoclonal antibodies show potent efficacy in psoriasis but poor effect in rheumatoid arthritis (RA) and Crohn's disease. Alternative agents targeting Th17 cells may be a better way to inhibit the development and function of Th17 cells than antibodies of blocking a single effector cytokine. Retinoic acid-related orphan receptor gamma t (RORγt) which acts as the master transcription factor of Th17 differentiation has been an attractive pharmacologic target for the treatment of Th17-mediated autoimmune disease. Recent progress in technology of chemical screen and engineering nucleic acid enable two new classes of therapeutics targeting RORγt. Chemical screen technology identified several small molecule specific inhibitors of RORγt from a small molecule library. Systematic evolution of ligands by exponential enrichment (SELEX) technology enabled target specific aptamers to be isolated from a random sequence oligonucleotide library. In this review, we highlight the development and therapeutic potential of small molecules inhibiting Th17 cells by targeting RORγt and aptamer mediated CD4(+) T cell specific delivery of small interference RNA against RORγt gene expression to inhibit pathogenic effector functions of Th17 lineage.

Indexed as

Cell DifferentiationDigoxinHeterocyclic Compounds, 4 or More RingsHumansNuclear Receptor Subfamily 1, Group F, Member 3PiperazinesPropanolsRNA, Small InterferingSELEX Aptamer TechniqueSulfonamidesTh17 CellsThiazolesTriterpenesUrsolic Acid1,1,1,3,3,3-hexafluoro-2-(2-fluoro-4'-((4-(pyridin-4-ylmethyl)piperazin-1-yl)methyl)-(1,1'-biphenyl)-4-yl)propan-2-olDigoxinHeterocyclic Compounds, 4 or More RingsNuclear Receptor Subfamily 1, Group F, Member 3PiperazinesPropanolsRNA, Small InterferingSR1001SulfonamidesThiazolesTMP778TriterpenesUrsolic Acid

Identifiers

PMID26792955
PMCPMC4697089
OpenAlexW2210677125

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.