Evidence map›Paper›PMID 26394814›Full record

ArticleJournal of leukocyte biology2016

Complement anaphylatoxin receptors C3aR and C5aR are required in the pathogenesis of experimental autoimmune uveitis.

Lingjun Zhang, Brent A Bell, Minzhong Yu, Chi-Chao Chan, Neal S Peachey, John Fung, Xiaoming Zhang, Rachel R Caspi, Feng Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  8. Review
  9. Article
  10. The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. CD55 Is Essential for CD103The American journal of pathology · 2019
    Article
  16. Retinal microglia initiate neuroinflammation in ocular autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

9 authors at 5 institutions in 2 countries.

Lingjun Zhang*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Brent A Bell*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Minzhong Yu*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Chi-Chao Chan*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Neal S Peachey*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
John Fung*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Xiaoming Zhang*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA linf2@ccf.org xzhang08@tmu.edu.cn.
Rachel R Caspi*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA.
Feng Lin*Eye Research Institute, Tianjin Medical University Eye Center, Tianjin, China; Department of Immunology, Lerner Research Institute, Department of Ophthalmic Research, Cole Eye Institute, and Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA; and Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA linf2@ccf.org xzhang08@tmu.edu.cn.
Cleveland Eye Clinic · USCleveland Clinic Lerner College of Medicine · USNational Eye Institute · USCleveland Clinic · USTianjin Medical University Eye Hospital · CN

Funding

Genetic, Cellular and Molecular Mechanisms in Autoimmunity to RetinaZIAEY000184 · NEI · NATIONAL EYE INSTITUTE · PI CASPI, RACHEL R. · 2009 to 2025
$51.7M
TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
Complement and OsteoporosisR01AR061564 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI DENNIS, JAMES E, LIN, FENG C · 2012 to 2015
$1.5M
BLRD VA IK6 BX005233NEI NIH HHS P30 EY011373NIAMS NIH HHS AR061564NIAMS NIH HHS R01 AR061564NIDDK NIH HHS DK10358
6 · The paper itself

Abstract

Recent studies have suggested that reagents inhibiting complement activation could be effective in treating T cell mediated autoimmune diseases such as autoimmune uveitis. However, the precise role of the complement anaphylatoxin receptors (C3a and C5a receptors) in the pathogenesis of autoimmune uveitis remains elusive and controversial. We induced experimental autoimmune uveitis in mice deficient or sufficient in both C3a and C5a receptors and rigorously compared their retinal phenotype using various imaging techniques, including indirect ophthalmoscopy, confocal scanning laser ophthalmoscopy, spectral domain optical coherence tomography, topical endoscopic fundus imaging, and histopathological analysis. We also assessed retinal function using electroretinography. Moreover, we performed Ag-specific T cell recall assays and T cell adoptive transfer experiments to compare pathogenic T cell activity between wild-type and knockout mice with experimental autoimmune uveitis. These experiments showed that C3a receptor/C5a receptor-deficient mice developed much less severe uveitis than did control mice using all retinal examination methods and that these mice had reduced pathogenic T cell responses. Our data demonstrate that both complement anaphylatoxin receptors are important for the development of experimental autoimmune uveitis, suggesting that targeting these receptors could be a valid approach for treating patients with autoimmune uveitis.

Indexed as

Adoptive TransferAnimalsAutoimmune DiseasesElectroretinographyMiceMice, Inbred C57BLMice, KnockoutReceptor, Anaphylatoxin C5aReceptors, ComplementTh17 CellsTh1 CellsUveitisC5ar1 protein, mousecomplement C3a receptorReceptor, Anaphylatoxin C5aReceptors, Complementinnate immunitymouse modelregulationretinal inflammationT cell

Identifiers

PMID26394814
PMCPMC6608042
OpenAlexW2267022665

What OpenQuestion holds

Textmetadata
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.