Bordetella pertussis, the causative agent of whooping cough, is forcefully reemerging wide world as a leading[AS1] cause of morbidity and mortality among infants. Th17 cells increase in response to this infection and are crucial in it's resolution. Here we study a subset of Th17 cells, 'Th17-like Tregs', that was recently described in several inflammatory models and test the hypothesis that this subset has a functional role in maintaining Th17 cell frequency and resolution of whooping cough. While lung Treg populations are relatively stable and minimally affected by PTX, Th17-like Tregs follow a frequency pattern similar to Th17 and rise in a robust and PTX-dependent manner in the late stages of infection. Phenotypic analyses show that Th17-like Tregs express similar regulatory features to Tregs, but also pathogenic characteristics such as IL-22 and IL-17, CXCR3, and CCR6. IFNa promotes T regulatory cell differentiation in vitro, but in Th17 polarizing conditions many of these Tregs acquire inflammatory characteristics such as RORgt and production of IL-17. Blocking IFNa in vivo leads to an expansion of T cell subsets that express IL-17, suggesting that IFNa has the capacity to inversely immunomodulate Tregs versus Th17. However, both cells types display plasticity and may acquire each other's characteristics. In vitro proliferation assays suggest that CD25high cells derived from late stage infection, remain functionally suppressive to naïve T cells although expressing pathogenic characteristics. This study will elucidate the role of Th17 Tregs in B. pertussis pathogenesis and expand our understanding of respiratory immune responses during respiratory infection.