Evidence map›Paper›PMID 42328437›Full record

ArticleInternational journal of biological sciences2026

Unveiling Interleukin-40: A Novel Regulator of Macrophage and B Cell Function in Allergic Asthma.

Aixuan Li, Katie Ching-Yau Wong, Danqi Huang, Fang Chen, Haoxuan Li, Xun Gao, Ting-Fan Leung, Gary Wing-Kin Wong, Wing-Hung Ko, Chun-Kwok Wong

Abstract read
In one paragraph

Article in International journal of biological sciences, 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

10 authors.

Aixuan LiSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Katie Ching-Yau WongDepartment of Chemical Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Danqi HuangDepartment of Chemical Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Fang ChenInstitute of Chinese Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Haoxuan LiDepartment of Chemistry, Department of Biochemistry and Molecular Biology, and Institute for Biophysical Dynamics, The University of Chicago, Chicago, IL, USA.
Xun GaoCenter of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University, Nanjing, Jiangsu, China.
Ting-Fan LeungDepartmenmt of Paediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Gary Wing-Kin WongDepartmenmt of Paediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Wing-Hung KoSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Chun-Kwok WongDepartment of Chemical Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic asthma is characterized by chronic airway inflammation and heightened type 2 immune responses. Although inhaled corticosteroids are the mainstay of therapy, a subset of patients exhibits suboptimal responses, underscoring the need for new therapeutic targets. In this study, we investigated the role of novel B cell-related interleukin-40 (IL-40) in allergic asthma using patient samples and a house dust mite (HDM)-induced mouse model. Through transcriptomic and immunological profiling, our findings revealed that IL-40 expression was significantly upregulated in both patients with allergic asthma and murine model. Elevated IL-40 levels exacerbated airway hyperresponsiveness (AHR), promoted inflammatory cell infiltration, and increased the production of type 2 cytokines, indicating a key role in amplifying allergic airway inflammation. Importantly, treatment with a neutralizing antibody against IL-40 or genetic deletion of IL-40 significantly alleviated airway inflammation, suggesting its therapeutic potential. Mechanistically, these pro-inflammatory effects of IL-40 were closely associated with alterations in macrophage polarization and B cell development. Macrophages exhibited the highest induction of IL-40 secretion following allergen exposure and responded most strongly to IL-40 stimulation. This response involved the activation of the JAK/STAT1 and p38-MAPK signaling pathways, driving their polarization toward a pro-inflammatory phenotype while inhibiting the differentiation of a specific Arg1

Indexed as

AsthmaB-LymphocytesInterleukin-1MacrophagesAnimalsFemaleHumansMiceInterleukin-1airway inflammationallergic asthmaB cellIL-40macrophage

Identifiers

PMID42328437
PMCPMC13282775

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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.