Type 2 Biomarkers in Asthma: Yet Another Reflection of Heterogeneity

T2 inflammation occurs along a continuum in the airways of patients with asthma, and these patients begin to exhibit specific clinical characteristics after exceeding a threshold of inflammatory cytokine expression.1,2 The surrogate markers used to determine underlying inflammation are highly variable and therefore need to be repeated to increase the accuracy of phenotypic characterization.3 This may be related to effects of triggers and therapies on both underlying inflammation and the associated biomarkers. The study population differed from those in several of the phase III studies for biologics in severe asthma in that the population was less obese, had a very high prevalence of nasal polyps (40% of assessed patients), and had on average fewer exacerbations and higher asthma control questionnaire scores.5,6 Therein lies the challenge in attempting to determine the prevalence of specific biomarkers in a population with severe asthma. There is no consensus on the description of this subtype, and it is likely that non-T2 asthma is equally heterogeneous with multiple underlying inflammatory mechanisms at play.8 The prevalence of non-T2 asthma may also differ in mild to moderate as compared with severe asthma, with some studies demonstrating that nearly two-third of patients with mild to moderate disease have persistent noneosinophilic inflammation.9 The goal of providing care in a precise and targeted manner cannot be realized until the tools we use to identify patients are sharpened, and this will likely require the use of advanced techniques to identify and refine asthma endotypes.