Evaluation of the lymphocyte responses to allergen is a useful delayed drug hypersensitivity diagnostic tool (10, 27–29). LST has long been used as a diagnostic tool for delayed hypersensitivity against several fungi (Table 2). The incorporation of tritiated thymidine was the gold standard for the detection of fungal-specific T cells. Owing to the constraints inherent to radioactive methods, new markers were developed, with CD69 and CD25 upregulation being the most popular (30–32). Currently, an alternative is the lymphocyte proliferation test with 5,6-carboxylfluorescein diacetate succinimidyl ester (CFSE) (33). Few studies have evaluated T helper (Th) 2 cytokine production after fungal stimulation, notably IL-5, for ABPM diagnosis (23, 24). Stimulation with Af extract and recombinant proteins in ABPA patients has shown an unusual Th2 immune response (34). Patients with invasive aspergillosis displayed a Th1 phenotype (35) and a Th17 phenotype (36), corresponding to a relevant anti-infectious immune activation. Taken together, these studies show that the immune skew present in a given patient's responses to fungal antigens can be evidenced through functional tests. However, the specificity of Th2 activation induced by fungal antigens as a diagnostic marker for ABPM has not been established, restricting the relevance of this method for ABPM diagnosis. Recently, a new method was developed, based on magnetic antigen-reactive T cell enrichment (ARTE) of CD154+ (CD40L+) T cells, which allowed the identification of rare populations of antigen-specific T cells. Briefly, after PBMC and antigen coculture, antigen-specific cells were sorted via magnetic beads, separating CD154+ conventional T (Tcon) cells from CD137+ CD154− regulatory T cells. Magnetic enrichment allowed an easy and detailed flow cytometry analysis of subpopulations (37). Tcon cells from lung immunocompromised patients showed a strong Th2 activation after fungal antigen stimulation (38). In our study, LST was not performant for ABPM diagnosis. Yet, our results suggest that LST might predict the development of ABPM. Indeed, the patient with the highest results in our cohort, presenting with a strong CD4 and CD8 T cell activation to fungal extracts, developed an ABPA 3 months after the abnormal LST assay. Detection of peripheral fungal-specific T cell, which can activate downstream humoral responses, may highlight a pathological process underlying subclinical ABPA with the potential of development of full-blown ABPA. A larger study with an extended follow-up will be essential to confirm this hypothesis.