ReviewCurrent opinion in allergy and clinical immunology2026
Reframing paucigranulocytic asthma through genetic endotyping: a hypothesis-generating focus on the 17q21 rs7216389 locus.
Review in Current opinion in allergy and clinical 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.
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Abstract
purpose of reviewNon-T2 asthma is currently defined by missing parameters, such as low blood eosinophils and FeNO, rather than positively identifiable mechanistic features. This definition overlaps with paucigranulocytic asthma (PGA). However, T2-biomarkers fluctuate over time, especially during glucocorticoid therapy, leading to potential over-diagnosis of T2-low asthma. Advancing beyond traditional endotyping is required for precision medicine. RECENT
findingsAlarmin-driven asthma [interleukin (IL)-33, thymic stromal lymphopoietin (TSLP), IL-25] can drive inflammation even without high T2-markers, but these are difficult to measure clinically. Genetic testing, such as the rs7216389 SNP (17q21 locus, GSDMB/ORMDL3), offers a stable alternative. The T allele is linked to childhood-onset asthma, viral-induced alarmin release, and epithelial dysfunction. Notably, carriers of the T allele are more likely to respond to allergen immunotherapy (AIT). This genetic marker is not subjected to treatment-dependent modification and segregates with both T2-driven and alarmin-driven asthma. SUMMARY: We propose that rs7216389 genotyping could be explored, within a treatable trait framework, to improve the mechanistic characterization of paucigranulocytic or low-biomarker asthma. While current data are associative, this one-time genetic assessment might contribute to research-driven stratification of "hidden" T2- or alarmin-leaning endotypes, potentially guiding the use of AIT and upstream biologics like anti-TSLP.
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