Evidence map›Paper›PMID 33347356›Full record

ArticlemAbs

Therapeutic blockade of CXCR2 rapidly clears inflammation in arthritis and atopic dermatitis models: demonstration with surrogate and humanized antibodies.

Md Jahangir Alam, Liang Xie, Caroline Ang, Farnaz Fahimi, Stephen B Willingham, Andrew J Kueh, Marco J Herold, Charles R Mackay, Remy Robert

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in mAbs. 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
2.0field-weighted citation impact, top 11% 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, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Neutrophils in chronic inflammatory diseases.Cellular & molecular immunology · 2022
    Review
  11. Article
  12. pH and Proton Sensor GPR65 Determine Susceptibility to Atopic Dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    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 3 institutions in 2 countries.

Md Jahangir AlamDepartment of Microbiology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.ORCID 0000-0002-7935-6346
Liang XieDepartment of Microbiology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.
Caroline AngDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.
Farnaz FahimiDepartment of Physiology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.
Stephen B WillinghamCorvus Pharmaceuticals , Burlingame, CA, USA.
Andrew J KuehWalter and Eliza Hall Institute of Medical Research , Parkville, Victoria, Australia.
Marco J HeroldWalter and Eliza Hall Institute of Medical Research , Parkville, Victoria, Australia.
Charles R MackayDepartment of Microbiology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.ORCID 0000-0002-6338-7340
Remy RobertDepartment of Physiology, Biomedicine Discovery Institute, Monash University , Clayton, Victoria, Australia.ORCID 0000-0003-2416-9268
Discovery Institute · USThe University of Melbourne · AUSilvus Technologies (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are the most abundant effector cells of the innate immune system and represent the first line of defense against infection. However, in many common pathologies, including autoimmune diseases, excessive recruitment and activation of neutrophils can drive a chronic inflammatory response leading to unwanted tissue destruction. Several strategies have been investigated to tackle pathologic neutrophil biology, and thus provide a novel therapy for chronic inflammatory diseases. The chemokine receptor CXCR2 plays a crucial role in regulating neutrophil homeostasis and is a promising pharmaceutical target. In this study, we report the discovery and validation of a humanized anti-human CXCR2 monoclonal antibody. To enable

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedArthritis, ExperimentalDermatitis, AtopicFemaleMiceMice, TransgenicReceptors, Interleukin-8BAntibodies, Monoclonal, HumanizedCXCR2 protein, humanReceptors, Interleukin-8Barthritisatopic DermatitisCXCR2inflammationneutrophiltherapeutic antibody

Identifiers

PMID33347356
PMCPMC7757791
OpenAlexW3113391648

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.