Evidence map›Paper›PMID 9151904›Full record

ArticleThe Journal of experimental medicine1997

Costimulation through B7-2 (CD86) is required for the induction of a lung mucosal T helper cell 2 (TH2) immune response and altered airway responsiveness.

S Tsuyuki, J Tsuyuki, K Einsle, M Kopf, A J Coyle

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 251 citations in OpenAlex.

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  6. Eosinophilia in cancer and its regulation by sex hormones.Trends in endocrinology and metabolism: TEM · 2023
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  12. Dual checkpoint inhibitor-associated eosinophilic enteritis.Journal for immunotherapy of cancer · 2019
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  13. Defective lung function following influenza virus is due to prolonged, reversible hyaluronan synthesis.Matrix biology : journal of the International Society for Matrix Biology · 2019
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  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Experimental advances in understanding allergic airway inflammation.Frontiers in bioscience (Scholar edition) · 2013
    Review
  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

5 authors at 1 institution in 1 country.

S TsuyukiR&D Dept. Kissei Pharmaceutical Co. Ltd., Matsumoto, Japan.
J Tsuyuki
K Einsle
M Kopf
A J Coyle
Kissei Pharmaceutical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recruitment of eosinophils into the airways after allergen exposure is dependent on interleukin (IL) 5 secreted from antigen-specific CD4+ T cells of the T helper cell (Th) 2 subset. However, while it is established that costimulation through CD28 is required for TCR-mediated activation and IL-2 production, the importance of this mechanism for the induction of a Th2 immune response is less clear. In the present study, we administered the fusion protein CTLA-4 immunoglobulin (Ig) into the lungs before allergen provocation to determine whether CD28/CTLA-4 ligands are required for allergen-induced eosinophil accumulation and the production of Th2 cytokines. Administration of CTLA-4 Ig inhibited the recruitment of eosinophils into the lungs by 75% and suppressed IgE in the bronchoalveolar lavage fluid. CTLA-4 Ig also inhibited the production of IL-4, IL-5, and IL-10 by 70-80% and enhanced interferon-gamma production from CD3-T cell receptor-activated lung Thy1.2+ cells. Allergen exposure upregulated expression of B7-2, but not B7-1, on B cells from the lung within 24 h. Moreover, airway administration of an anti-B7-2 monoclonal antibody (mAb) inhibited eosinophil infiltration, IgE production, and Th2 cytokine secretion comparable in magnitude to that observed with CTLA-4 Ig. Treatment with an anti-B7-1 mAb had a small, but significant effect on eosinophil accumulation, although was less effective in inhibiting Th2 cytokine production. The anti-B7-2, but not anti-B7-1, mAb also inhibited antigen-induced airway hyperresponsiveness in vivo. In all of the parameters assessed, the combination of both the anti-B7-1 and anti-B7-2 mAb was no more effective than anti-B7-2 mAb treatment alone. We propose that strategies aimed at inhibition of CD28 interactions with B7-2 molecules may represent a novel therapeutic target for the treatment of lung mucosal allergic inflammation.

Indexed as

Immunity, MucosalImmunoconjugatesAbataceptAllergensAnimalsAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCells, CulturedChemotaxis, LeukocyteCTLA-4 AntigenCytokinesEosinophilsImmunoglobulin EAbataceptAllergensAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCd86 protein, mouseCTLA-4 AntigenCtla4 protein, mouseCytokinesImmunoconjugatesImmunoglobulin EInterferon-gammaMembrane Glycoproteins

Identifiers

PMID9151904
PMCPMC2196297
OpenAlexW2128085654

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.