Evidence map›Paper›PMID 42028242›Full record

ReviewThe World Allergy Organization journal2026

Overview of allergic disease: Pathogenesis of allergic inflammation - WAO White Book on Allergy 2026 - 2.1.

Luis Caraballo, Kevin Llinás-Caballero

Abstract readReview
In one paragraph

Review in The World Allergy Organization journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Luis CaraballoInstitute for Immunological Research, University of Cartagena, Cartagena de Indias, Colombia.
Kevin Llinás-CaballeroInstitute for Immunological Research, University of Cartagena, Cartagena de Indias, Colombia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic inflammation underlies several diseases such as asthma, rhinitis, and atopic dermatitis). It involves a great array of cells and molecules of innate and adaptive immunity. Components of the innate inflammatory pathways, among them epithelium receptors, alarmins and ILC2, are the earliest participants in some inflammatory processes, mainly the house dust mite induced bronchial inflammation in asthma. The importance of innate mechanisms, not only as a necessary step for inducing adaptive Th2 response but also to maintain chronic inflammation, is being increasingly recognized in recent years. In addition, the specificity of the Th2 cells and IgE is not only a crucial component of allergic inflammation but allows also identification of the causal inducers and their effects on eosinophils, neutrophils, and basophils recruitment and activation. The regulatory mechanisms of the allergic responses include Treg and Breg activity but the most important action to control this process is stopping the specific allergen exposure. However, this is very difficult to achieve in asthma because, in general, not all the allergens involved can be identified; in addition, non-immune pathways play also a role. Since most people exposed to proallergic environments do not develop allergic diseases and it is well known that these conditions run in families, their genetic and epigenetic influences are a matter of intensive research. In this review we make an update of the basic mechanisms of allergic inflammation, trying to identify important pathways that involve both innate and adaptive immunity, including environmental factors that can modify important regulators of immunity such as intestinal microbiota and air pollution.

Indexed as

AllergyAsthmaBlomia tropicalisDermatophagoides pteronyssinusHouse dust miteIgEILC2InflammationType-2 immunity

Identifiers

PMID42028242
PMCPMC13100273

What OpenQuestion holds

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Registered trials

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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.