ArticleFrontiers in immunology2023
Multimodal analysis of granulocytes, monocytes, and platelets in patients with cystic fibrosis before and after Elexacaftor-Tezacaftor-Ivacaftor treatment.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 15 citations in OpenAlex.
- CFTR modulators exert subset-specific phenotype remodeling on circulating neutrophils in cystic fibrosis.ImmunoHorizons · 2026Article
- Comparison of the Effect of CFTR ModulatorsJournal of clinical medicine · 2025Article
- Blood platelet reduction after elexacaftor/tezacaftor/ivacaftor treatment in people with cystic fibrosis may depend on systemic inflammation reduction.Scientific reports · 2025Article
- Epithelial extracellular vesicles induce inflammation and neutrophil activation in theFrontiers in immunology · 2025Article
- Proteomics profiling of inflammatory responses to elexacaftor/tezacaftor/ivacaftor in cystic fibrosis.Frontiers in immunology · 2025Article
- Multimodal monitoring of neutrophil activity during cardiac surgery.Frontiers in immunology · 2025Article
- Wound repair and immune function in theFrontiers in cellular and infection microbiology · 2025Review
- Biochemical assessment in a cohort of pediatric patients with cystic fibrosis.Journal of medicine and life · 2024Article
- Review
- Elevated level of serum human epididymis protein 4 (HE4) predicts disease severity and mortality in COVID-19 pneumonia.BMC pulmonary medicine · 2023Article
- Review
- Modulator-refractory cystic fibrosis: Defining the scope and challenges of an emerging at-risk population.Therapeutic advances in respiratory diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis (CF) is a monogenetic disease caused by an impairment of the cystic fibrosis transmembrane conductance regulator (CFTR). CF affects multiple organs and is associated with acute and chronic inflammation. In 2020, Elexacaftor-Tezacaftor-Ivacaftor (ETI) was approved to enhance and restore the remaining CFTR functionality. This study investigates cellular innate immunity, with a focus on neutrophil activation and phenotype, comparing healthy volunteers with patients with CF before (T1, n = 13) and after six months (T2, n = 11) of ETI treatment. ETI treatment reduced sweat chloride (T1: 95 mmol/l (83|108) vs. T2: 32 mmol/l (25|62), p < 0.01, median, first|third quartile) and significantly improved pulmonal function (FEV
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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.