ReviewEuropean journal of immunology2026
The Respiratory Epithelial Barrier as an Immunopharmacological Rheostat: From Homeostatic Sentinel to Therapeutic Target in Chronic Lung Disease.
Review in European journal of immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The Respiratory Epithelial Barrier as an Immunopharmacological Rheostat: From Homeostatic Sentinel to Therapeutic Target in Chronic Lung Disease.European journal of immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The respiratory epithelium is a dynamic immunopharmacological interface that transcends its traditional role as a passive barrier to become a central coordinator of pulmonary immunity. This review introduces and elaborates on the paradigm of the "Epithelial Immunopharmacological Rheostat," a conceptual framework that posits the epithelium as a dynamic, multidimensional signal processor that continuously calibrates the threshold of immune activation. Distinct from static models of barrier dysfunction or isolated alarmin biology, this rheostat operates through four hierarchically interacting axes: barrier integrity, alarmin/type 2, senescence/repair, and tolerogenic programming. We critically dissect how dysregulation of specific axes-alone or in combination-initiates and perpetuates the pathology of chronic respiratory diseases, including asthma, COPD, and idiopathic pulmonary fibrosis. A rigorous, pharmacology-centric analysis deconstructs the molecular circuitry of epithelial-immune crosstalk, evaluating the druggability of targets from tight junction complexes and pattern recognition receptors to the alarmin (TSLP, IL-33, IL-25) signaling cascades and their downstream JAK-STAT, NF-κB, and MAPK effectors. Beyond cataloguing mechanisms, this review provides a comparative and critical appraisal of emerging therapeutic strategies, including alarmin-targeted biologics, barrier-restorative agents (e.g., postbiotics, short-chain fatty acids), kinase inhibitors, senotherapeutics, and frontier cell-based therapies. A dedicated synthesis addresses pivotal pharmacokinetic hurdles, biomarker-driven stratification, and the imperative of precision endotyping. Finally, we forecast how advanced human organoid models are catalyzing the shift toward personalized interventions designed to reset the defective rheostat. This comprehensive synthesis maps the intricate landscape of epithelial immunopharmacology and identifies critical barriers that must be overcome to translate these insights into transformative clinical outcomes.
Indexed as
Identifiers
What Socratic 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 Socratic graph.