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Article

Type-2-Inflammatory-Diseases Share Comorbidities, Molecular Signatures, IL4/IL13 Genetics, and Response to IL4/IL13 Blockade.

Allergy - 1 Sept 2026

Hamilton Jennifer D, Ferreira Manuel A R, Lim Wei Keat, Sidore Carlo, Wipperman Matthew F, Ge Wenzhen, Song Xue, Xia Changming, Horowitz Julie E, Hooper Andrea T, Hamon Sara C, Maloney Jennifer, Orengo Jamie M, Chen Zhen, Ricci Stephanie Amato, Akinlade Bolanle, Baras Aris, Herman Gary, Bennett Brandy L, Yancopoulos George D

Abstract excerpt

BACKGROUND: It has long been appreciated that multiple allergic/atopic conditions (type-2-inflammation-associated diseases, T2IDs) often appear in the same individual, suggesting a shared systemic immune deviation. Emerging molecular and clinical investigations of interleukin (IL)4/IL13 blockade with the fully-human antibody dupilumab suggest that many are driven by over-activation of the IL4/IL13 pathway,...

Read the complete abstract on PubMed

Topics

Humans
Interleukin-13
Interleukin-4
Genetic Predisposition to Disease

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Comorbidity

Inflammation

Antibodies, Monoclonal, Humanized

Gene Expression Profiling

Source

Open in PubMed Open full text

Identifiers

PMID: 42135900
DOI: 10.1111/all.70380
PMCID: PMC13569704

Genes

IL13
IL4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 25 Oct 2026.

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