ReviewFrontiers in immunology2026
Immune-inflammatory endotypes of chronic rhinosinusitis: from epithelial alarmins to personalized therapy.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic rhinosinusitis (CRS) is a prevalent and complex inflammatory disease within otolaryngology, traditionally classified into phenotypes based on the presence (CRSwNP) or absence (CRSsNP) of nasal polyps. However, these phenotypic classifications inadequately capture the underlying pathophysiological heterogeneity of CRS. Recently, immune-inflammatory endotyping has emerged as a pivotal approach to better characterize CRS by delineating distinct inflammatory pathways, primarily type 1, type 2, and type 3 immune responses, each driven by unique immune cells and cytokine profiles. Epithelial-derived cytokines such as thymic stromal lymphopoietin (TSLP), IL-33, and IL-25, alongside immune cells including group 2 innate lymphoid cells (ILC2), T helper 2 (Th2), and Th17 cells, play critical roles in modulating the immune landscape of CRS. Moreover, variations in immune responses among different populations highlight the disease's heterogeneity and underscore the need for precise immunological characterization. This review comprehensively summarizes recent advances in the immune-inflammatory endotyping of CRS, elucidates the underlying immunopathogenic mechanisms, and discusses the clinical significance of these endotypes. By integrating current research findings, this article aims to provide a theoretical foundation for the development of personalized therapeutic strategies tailored to distinct immune-inflammatory profiles in CRS patients.
Indexed as
Identifiers
What OpenQuestion holds
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.