Type I interferons (IFNs) play a complex role in the immune response to infectious diseases, with both protective and detrimental effects depending on the context. They are crucial for host defense against viruses, but can also cause immune pathology in acute infections and lead to immune suppression in chronic infections. During bacterial infections, type I IFNs may be required early to initiate cell-mediated immunity, but high concentrations can block B cell responses and reduce macrophage responsiveness to IFNγ. Recent studies have shown that cytokine networks, such as those involving prostaglandin E2 and interleukin-1, can regulate type I IFN expression to minimize host damage. Type I IFNs are produced by various cells in response to pathogen recognition receptors, which detect microbial components. The induction of IFNα/β involves a cascade of signaling pathways, including the activation of IRF3 and IRF7, which drive the transcription of IFN genes. IFNα/β signal through the IFNAR receptor, activating JAK-STAT pathways and leading to the expression of IFN-stimulated genes (ISGs) that confer antiviral effects. However, IFNα/β signaling is not limited to the canonical pathway and can involve other STATs and signaling molecules, contributing to a broad range of immune responses. In viral infections, IFNα/β are essential for restricting viral replication by inducing an antiviral state in cells. They also enhance the function of dendritic cells, monocytes, and T and B cells, promoting adaptive immune responses. However, in chronic infections, IFNα/β can suppress immune responses, leading to impaired viral control. In acute infections like influenza, excessive IFNα/β can cause immunopathology by inducing apoptosis and inflammation, contributing to tissue damage. In bacterial infections, the role of IFNα/β is more variable. While they can be protective by enhancing macrophage function and promoting antibacterial effector mechanisms, they can also be detrimental by suppressing immune responses and increasing susceptibility to certain pathogens. For example, in infections with *L. monocytogenes* and *M. tuberculosis*, IFNα/β can impair macrophage activation and reduce the ability to control bacterial growth. Overall, the effects of type I IFNs are highly context-dependent, influenced by the type of pathogen, the stage of infection, and the specific immune cell responses involved. Understanding these complex interactions is crucial for developing therapeutic strategies to modulate IFN responses in infectious diseases.Type I interferons (IFNs) play a complex role in the immune response to infectious diseases, with both protective and detrimental effects depending on the context. They are crucial for host defense against viruses, but can also cause immune pathology in acute infections and lead to immune suppression in chronic infections. During bacterial infections, type I IFNs may be required early to initiate cell-mediated immunity, but high concentrations can block B cell responses and reduce macrophage responsiveness to IFNγ. Recent studies have shown that cytokine networks, such as those involving prostaglandin E2 and interleukin-1, can regulate type I IFN expression to minimize host damage. Type I IFNs are produced by various cells in response to pathogen recognition receptors, which detect microbial components. The induction of IFNα/β involves a cascade of signaling pathways, including the activation of IRF3 and IRF7, which drive the transcription of IFN genes. IFNα/β signal through the IFNAR receptor, activating JAK-STAT pathways and leading to the expression of IFN-stimulated genes (ISGs) that confer antiviral effects. However, IFNα/β signaling is not limited to the canonical pathway and can involve other STATs and signaling molecules, contributing to a broad range of immune responses. In viral infections, IFNα/β are essential for restricting viral replication by inducing an antiviral state in cells. They also enhance the function of dendritic cells, monocytes, and T and B cells, promoting adaptive immune responses. However, in chronic infections, IFNα/β can suppress immune responses, leading to impaired viral control. In acute infections like influenza, excessive IFNα/β can cause immunopathology by inducing apoptosis and inflammation, contributing to tissue damage. In bacterial infections, the role of IFNα/β is more variable. While they can be protective by enhancing macrophage function and promoting antibacterial effector mechanisms, they can also be detrimental by suppressing immune responses and increasing susceptibility to certain pathogens. For example, in infections with *L. monocytogenes* and *M. tuberculosis*, IFNα/β can impair macrophage activation and reduce the ability to control bacterial growth. Overall, the effects of type I IFNs are highly context-dependent, influenced by the type of pathogen, the stage of infection, and the specific immune cell responses involved. Understanding these complex interactions is crucial for developing therapeutic strategies to modulate IFN responses in infectious diseases.