ArticleJournal of immunology (Baltimore, Md. : 1950)2025
Cutting edge: Extrinsic and intrinsic sex effects differentially regulate pulmonary ILC2 numbers, phenotype, and function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Androgens protect ILC2S from functional suppression during influenza virus infection.Mucosal immunology · 2026Article
- Grand challenges in sex differences in immunology: problems the field must solve before biological sex can guide clinical practice.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Pulmonary type 2 innate lymphocytes (ILC2s) show sex dimorphism in numbers, phenotype, and function. We used a novel strategy of competitive, mixed male-female donor bone marrow chimeras to determine if sex differences in murine ILC2s result from extrinsic factors in the recipient environment or from durable intrinsic variables in donor cells. We show that the recipient sex environment regulated ILC2 numbers and IL33R/ST2 and KLRG1 surface levels, independent of donor sex. In contrast, ILC2 production of interleukin (IL)-5 depended on donor cell sex and the type of inflammatory stimulus. After allergen exposure, or upon treatment of naïve lung cells with PMA/ionomycin, a higher frequency of female donor-derived ILC2s produced IL-5. In contrast, influenza virus infection induced a greater proportion of male donor-derived ILC2s to produce IL-5. Thus, while a current sex environment governed pulmonary ILC2 numbers and canonical markers, ILC2 functional responses were shaped by durable factors stemming from intrinsic biological sex.
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Registered trials
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.