Evidence map›Paper›PMID 20398663›Full record

ArticleGastroenterology2010

Paired immunoglobulin-like receptor B (PIR-B) negatively regulates macrophage activation in experimental colitis.

Ariel Munitz, Eric T Cole, Amanda Beichler, Katherine Groschwitz, Richard Ahrens, Kris Steinbrecher, Tara Willson, Xiaonan Han, Lee Denson, Marc E Rothenberg and 1 more

Abstract read
In one paragraph

Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  16. PIR-B Regulates CD4Cellular and molecular gastroenterology and hepatology · 2021
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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

11 authors at 2 institutions in 2 countries.

Ariel MunitzDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
Eric T Cole
Amanda Beichler
Katherine Groschwitz
Richard Ahrens
Kris Steinbrecher
Tara Willson
Xiaonan Han
Lee Denson
Marc E Rothenberg
Simon P Hogan
Cincinnati Children's Hospital Medical Center · USTel Aviv University · IL

Funding

Unique Effects of IL-13 in Asthma: Mechanistic AnalysisP01HL076383 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2004 to 2008
$10.1M
Interleukin-9 In Experimental Intestinal AnaphylaxisR01AI073553 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HOGAN, SIMON PATRICK · 2008 to 2011
$1.5M
Eosinophil, Chemokine and IL-13 Cooperativity in AsthmaR01AI057803 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2004 to 2007
$731k
NHLBI NIH HHS P01 HL-076383NHLBI NIH HHS P01 HL076383NIAID NIH HHS R01 AI057803NIAID NIH HHS R01 AI073553NIAID NIH HHS R01 AI073553-01
6 · The paper itself

Abstract

BACKGROUND &

aimsInnate and adaptive immune responses are regulated by cross talk between activation and inhibitory signals. Dysregulation of the inhibitory signal can lead to aberrant chronic inflammatory diseases such as the inflammatory bowel diseases (IBD). Little is known about negative regulation of innate intestinal immune activation. We examined the role of the inhibitory receptor paired immunoglobulin-like receptor B (PIR-B) in the regulation of macrophage function in innate intestinal immunity.

methodsWe examined the susceptibility of Pirb-/- and wild-type (WT) mice to dextran sodium sulfate (DSS)-induced colitis. We assessed proinflammatory cytokine release and mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB) activation in Pirb-/- and WT macrophages following Escherichia coli stimulation. Macrophage transfer experiments were performed to define the role of PIR-B in the negative regulation of macrophage function in DSS-induced colitis. We also assessed expression of PIR-B human homologues (immunoglobulin-like transcript [ILT]-2 and ILT-3) in colon biopsy samples from healthy individuals (controls) and patients with IBD.

resultsPirb-/- mice had increased susceptibility to DSS-induced colitis. In vitro analysis showed increased production of proinflammatory cytokines (interleukin-6, interleukin-1beta, and tumor necrosis factor alpha) and activation of MAPK and NF-kappaB in Pirb-/- macrophages following bacterial activation. Adoptive transfer of bone marrow-derived Pirb-/- macrophages into WT mice was sufficient to increase disease susceptibility. ILT-2 and ILT-3 were expressed on CD68+ and CD68- mononuclear cells and intestinal epithelium in colon biopsy samples from patients and controls.

conclusionsPIR-B negatively regulates macrophage functions in response to pathogenic bacteria and chronic intestinal inflammatory responses. Inhibitory receptors such as PIR-B might be used as therapeutic targets for treatment of patients with IBD.

Indexed as

Immunity, InnateMacrophage ActivationAdolescentAdoptive TransferAnimalsAntigens, CDBiopsyCase-Control StudiesChildChild, PreschoolColitisColonCytokinesDextran SulfateDisease Models, AnimalEscherichia coliAntigens, CDCytokinesDextran SulfateInflammation MediatorsLeukocyte Immunoglobulin-like Receptor B1LILRB1 protein, humanLILRB4 protein, humanMembrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa BPirb protein, mouseProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Ptpn11 protein, mousePtpn6 protein, mouseReceptors, Cell SurfaceReceptors, Immunologic

Identifiers

PMID20398663
PMCPMC3423916
OpenAlexW2027351375

What OpenQuestion holds

Textmetadata
LicenceTDM
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.