S. pyogenes also known as Group A Streptoccocus (GAS) is a common human pathogen responsible of a variety of diseases that range from mild pharyngitis to rare but invasive and life-threatening infections. We have demonstrated that type I interferon (IFN) signaling is required for mice survival in a model of subcutaneous infection with S. pyogenes. However, it is not understood how these cytokines are induced and how they protect the host. Using mice deficient in the type I IFN receptor IFNAR1 we observed increased tissue damage at the site of infection despite similar bacterial loads in the absence of type I IFN signaling. IFNAR1-deficient mice exhibit hyperinflammation with increased levels of IL-1ß in the infected tissue and in the liver and spleen. Excessive IL-1ß production seems to promote organ injury as confirmed by the histology analysis and by the levels of transaminases and other parameters measured in the blood. On the other hand, IL-1ß signaling is essential for mouse survival during infection with S. pyogenes since mice lacking the IL-1 receptor or Caspase-1, the key IL-1ß-processing enzyme, are highly susceptible to S. pyogenes infection. Together, our data provide evidence that type I IFNs are essential for balancing the immune response against S. pyogenes and that the absence of type I IFN signaling results in lethal systemic hyperinflammation accompanied by overproduction of IL-1b.