Evidence map›Paper›PMID 17290046›Full record

ArticleAmerican journal of respiratory and critical care medicine2007

CD48 is critically involved in allergic eosinophilic airway inflammation.

Ariel Munitz, Ido Bachelet, Fred D Finkelman, Marc E Rothenberg, Francesca Levi-Schaffer

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Fine-Tuning Group 2 Innate Lymphoid Cells: CD48 Pumps Up the Volume.American journal of respiratory cell and molecular biology · 2026
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  12. Roles of CD48 in regulating immunity and tolerance.Clinical immunology (Orlando, Fla.) · 2016
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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

5 authors at 3 institutions in 2 countries.

Ariel MunitzDepartment of Pharmacology, School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.
Ido Bachelet
Fred D Finkelman
Marc E Rothenberg
Francesca Levi-Schaffer
Hebrew University of Jerusalem · ILCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

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
REGULATION OF GASTROINTESTINAL EOSINOPHILSR01AI045898 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 1999 to 2024
$4.5M
MECHANISMS OF EOSINOPHILIA IN EXPERIMENTAL ASTHMAR01AI042242 · NIAID · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI ROTHENBERG, MARC E. · 1998 to 2002
$729k
NHLBI NIH HHS P01 HL076383-01NIAID NIH HHS R01 AI42242NIAID NIH HHS R01 AI45898
6 · The paper itself

Abstract

rationaleDespite ongoing research, the molecular mechanisms controlling asthma are still elusive. CD48 is a glycosylphosphatidylinositol-anchored protein involved in lymphocyte adhesion, activation, and costimulation. Although CD48 is widely expressed on hematopoietic cells and commonly studied in the context of natural killer and cytotoxic T cell functions, its role in helper T cell type 2 settings has not been examined.

objectivesTo evaluate the expression and function of CD48, CD2, and 2B4 in a murine model of allergic eosinophilic airway inflammation.

methodsAllergic eosinophilic airway inflammation was induced by ovalbumin (OVA)-alum sensitization and intranasal inoculation of OVA or, alternatively, by repeated intranasal inoculation of Aspergillus fumigatus antigen in wild-type, STAT (signal transducer and activator of transcription)-6-deficient, and IL-4/IL-13-deficient BALB/c mice. Gene profiling of whole lungs was performed, followed by Northern blot and flow cytometric analysis. Anti-CD48, -CD2, and -2B4 antibodies were administered before OVA challenge and cytokine expression and histology were assessed. MEASUREMENTS AND MAIN

resultsMicroarray data analysis demonstrated upregulation of CD48 in the lungs of OVA-challenged mice. Allergen-induced CD48 expression was independent of STAT-6, IL-13, and IL-4. Neutralization of CD48 in allergen-challenged mice abrogated bronchoalveolar lavage fluid and lung inflammation. Neutralization of CD2 inhibited the inflammatory response to a lesser extent and neutralization of 2B4 had no effect.

conclusionsOur results suggest that CD48 is critically involved in allergic eosinophilic airway inflammation. As such, CD48 may provide a new potential target for the suppression of asthma.

Indexed as

AnimalsAntigens, CDCD2 AntigensCD48 AntigenCytokinesDisease Models, AnimalMembrane GlycoproteinsMiceMice, Inbred BALB CMice, TransgenicPulmonary EosinophiliaReceptors, ImmunologicRespiratory HypersensitivityRNA, MessengerSignaling Lymphocytic Activation Molecule FamilyAntigens, CDCd244a protein, mouseCD2 AntigensCD48 AntigenCd48 protein, mouseCytokinesMembrane GlycoproteinsReceptors, ImmunologicRNA, MessengerSignaling Lymphocytic Activation Molecule Family

Identifiers

PMID17290046
PMCPMC1899297
OpenAlexW1977159931

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.