In conclusion, our data provide evidence that both asthma phenotypes share common immune-pathologic mechanisms, with expansion of CD26−/low subsets in AA (CD4+ Tlow or “highly-differentiated” Teff cells) and NAA (CD4− T cells; γδ-T lymphocytes) and down-modulation of additional surface molecules (IL-6Rα/CD126, CD27, CD28, IL-7Rα/CD127, CCR7) to produce differentiated effector subsets and extracellular sCD26 reduction. Here, CD28 is linked to asthma.