We developed an artificial intelligence algorithm (AIA) for smartphones to determine the severity of facial acne using the GEA scale and to identify different types of acne lesion (comedonal, inflammatory) and postinflammatory hyperpigmentation (PIHP) or residual hyperpigmentation. Overall, 5972 images (face, right and left profiles) obtained with smartphones (IOS and/or Android) from 1072 acne patients were collected. Three trained dermatologists assessed the acne severity for each patient. One acne severity grade per patient (grade given by the majority of the three dermatologists from the two sets of three images) was used to train the algorithm. Acne lesion identification was performed from a subgroup of 348 images using a tagging tool; tagged images served to train the algorithm. The algorithm evolved and was adjusted for sensibility, specificity and correlation using new images. The correlation between the GEA grade and the quantification and qualification of acne lesions both by the AIA and the experts for each image were evaluated for all AIA versions. At final version 6, the GEA grading provided by AIA reached 68% and was similar to that provided by the dermatologists. Between version 4 and version 6, AIA improved precision results multiplied by 1.5 for inflammatory lesions, 2.5 for non‐inflammatory lesions and by 2 for PIHP; recall was improved by 2.6, 1.6 and 2.7. The weighted average of precision and recall or F1 score was 84% for inflammatory lesions, 61% for non‐inflammatory lesions and 72% for PIHP.

T helper 9 (T_H9) cells promote allergic tissue inflammation and express the type 2 cytokines, IL-9 and IL-13, as well as the transcription factor, PPAR-γ. However, the functional role of PPAR-γ in human T_H9 cells remains unknown. Here, we demonstrate that PPAR-γ drives activation-induced glycolysis, which, in turn, promotes the expression of IL-9, but not IL-13, in an mTORC1-dependent manner. In vitro and ex vivo experiments show that the PPAR-γ-mTORC1-IL-9 pathway is active in T_H9 cells in human skin inflammation. Additionally, we find dynamic regulation of tissue glucose levels in acute allergic skin inflammation, suggesting that in situ glucose availability is linked to distinct immunological functions in vivo. Furthermore, paracrine IL-9 induces expression of the lactate transporter, MCT1, in T_H cells and promotes their aerobic glycolysis and proliferative capacity. Altogether, our findings uncover a hitherto unknown relationship between PPAR-γ-dependent glucose metabolism and pathogenic effector functions in human T_H9 cells.