Type I interferon (IFN‐α/β) is comprised of a family of highly related molecules that exert potent antiviral activity by interfering with virus replication and spread. IFN‐α/β secretion is tightly regulated through pathogen sensing pathways that are operative in most somatic cells. However, specialized antigen‐presenting plasmacytoid dendritic cells are uniquely equipped with the capacity to secrete extremely high levels of IFN‐α/β, suggesting a key role for this cytokine in priming adaptive T‐cell responses. Recent studies in both mice and humans have demonstrated a role for IFN‐α/β in directly influencing the fate of both CD4⁺ and CD8⁺ T cells during the initial phases of antigen recognition. As such, IFN‐α/β, among other innate cytokines, is considered an important ‘third signal’ that shapes the effector and memory T‐cell pool. Moreover, IFN‐α/β also serves as a counter‐regulator of T helper type 2 and type 17 responses, which may be important in the treatment of atopy and autoimmunity, and in the development of novel vaccine adjuvants.