As reported herein, our studies demonstrate that the ketone bodies AcAc and BHB inhibit agonist-induced cytokine production from several asthma-relevant cell types, including proinflammatory cytokine production from macrophages and airway epithelial cells, secretion of prototypic cytokines from polyclonally stimulated or restimulated CD4+ T cells, and type 2 cytokines and IFN-γ secretion from HDM allergen–restimulated lymphocyte cultures. This evidence concerns the gene CD4 and asthma.