Evidence map›Paper›PMID 31447855›Full record

ArticleFrontiers in immunology2019

C5a/C5aR1 Pathway Is Critical for the Pathogenesis of Psoriasis.

Quan-You Zheng, Shen-Ju Liang, Feng Xu, Gui-Qing Li, Na Luo, Shun Wu, You Li, Ming Tang, Yu Zhong, Jian Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The mRNA Expression Profile of Psoriatic Lesion Distinct from Non-Lesion.Clinical, cosmetic and investigational dermatology · 2022
    Article
  9. The role of C5a-C5aR1 axis in bone pathophysiology: A mini-review.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Article
  12. 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

14 authors at 2 institutions in 1 country.

Quan-You ZhengDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Shen-Ju LiangDepartment of Rheumatism and Immunology, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Feng XuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Gui-Qing LiDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Na LuoDepartment of Dermatology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Shun WuDepartment of Nephrology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
You LiDepartment of Nephrology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Ming TangDepartment of Nephrology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Yu ZhongDepartment of Urology, 958th Hospital of PLA, Army Medical University (Third Military Medical University), Chongqing, China.
Jian ChenDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Di YangDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Dao-Dong SunDepartment of Urology, 958th Hospital of PLA, Army Medical University (Third Military Medical University), Chongqing, China.
Ke-Qin ZhangDepartment of Nephrology, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Gui-Lian XuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is one of the most common chronic inflammatory skin diseases, affecting ~2% of the population. The lack of characterization of the pathogenesis of psoriasis has hindered efficient clinical treatment of the disease. In our study, we observed that expression of complement component 5a receptor 1(C5aR1) was significantly increased in skin lesions of both imiquimod (IMQ) and IL23-induced psoriatic mice and patients with psoriasis. C5aR1 deficiency or treatment with C5a receptor 1 antagonist (C5aR1a) in mice significantly attenuated psoriasis-like skin lesions and expression of inflammatory cytokines and chemokines. Moreover, C5aR1 deficiency significantly decreased IMQ-induced infiltration of plasmacytoid dendritic cells (pDCs), monocytes and neutrophils in psoriatic skin lesions and functions of pDCs, evidenced by the remarkable reduction in the IMQ-induced production of interferon-α (IFN-α) and tumor necrosis factor α (TNF-α), and FMS-like tyrosine kinase 3 ligand (FLT3L)-dependent pDCs differentiation. Accordingly,

Indexed as

AnimalsComplement C5aDendritic CellsHumansMiceMice, Inbred BALB CPsoriasisReceptor, Anaphylatoxin C5aComplement C5aReceptor, Anaphylatoxin C5aC5a/C5aR1complement systeminflammationmouse modelspsoriasis

Identifiers

PMID31447855
PMCPMC6692472
OpenAlexW2964208498

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.