Evidence map›Paper›PMID 38781017›Full record

ArticleJCI insight2024

Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution.

Liang Chen, Suresh Patil, Jeffrey Barbon, James Waire, Stephen Laroux, Donna McCarthy, Mishra Pratibha, Suju Zhong, Feng Dong, Karin Orsi and 11 more

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

21 authors.

Liang ChenAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Suresh PatilAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Jeffrey BarbonAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
James WaireAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Stephen LarouxAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Donna McCarthyAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Mishra PratibhaAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Suju ZhongAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Feng DongAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Karin OrsiAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Gunarso NguyenAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Yingli YangAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Nancy CrosbieAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Eric DominguezAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Arun DeoraAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Geertruida VeldmanAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Susan WestmorelandAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Liang JinAbbVie Bioresearch Center, Worcester, Massachusetts, USA.
Timothy RadstakeAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Kevin WhiteAbbVie, Cambridge Research Center, Cambridge, Massachusetts, USA.
Hsi-Ju WeiAbbVie Bay Area, South San Francisco, California, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DC inhibitory receptor (DCIR) is a C-type lectin receptor selectively expressed on myeloid cells, including monocytes, macrophages, DCs, and neutrophils. Its role in immune regulation has been implicated in murine models and human genome-wide association studies, suggesting defective DCIR function associates with increased susceptibility to autoimmune diseases such as rheumatoid arthritis, lupus, and Sjögren's syndrome. However, little is known about the mechanisms underlying DCIR activation to dampen inflammation. Here, we developed anti-DCIR agonistic antibodies that promote phosphorylation on DCIR's immunoreceptor tyrosine-based inhibitory motifs and recruitment of SH2 containing protein tyrosine phosphatase-2 for reducing inflammation. We also explored the inflammation resolution by depleting DCIR+ cells with antibodies. Utilizing a human DCIR-knock-in mouse model, we validated the antiinflammatory properties of the agonistic anti-DCIR antibody in experimental peritonitis and colitis. These findings provide critical evidence for targeting DCIR to develop transformative therapies for inflammatory diseases.

Indexed as

InflammationSignal TransductionAnimalsColitisDisease Models, AnimalHumansMiceMice, Inbred C57BLPeritonitisPhosphorylationAutoimmune diseasesAutoimmunityCellular immune responseImmunologyInnate immunity

Identifiers

PMID38781017
PMCPMC11383175

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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.