The article provides an overview of the structure and signaling mechanisms of the IL-17 receptor superfamily, focusing on the unique features and functions of IL-17A and its receptor (IL-17RA). IL-17A, a hallmark cytokine of T helper 17 (T<H17) cells, plays a dual role in protecting against extracellular pathogens and promoting inflammatory pathology in autoimmune diseases. The IL-17R family, including IL-17RA and other receptor subunits, has distinct structural features and signaling pathways that differ from those of other cytokine subclasses. IL-17A and IL-17F, the best-characterized members of the IL-17 family, activate pro-inflammatory pathways through a novel ACT1-dependent pathway, leading to the activation of NF-κB, a key transcription factor associated with inflammation. The article also discusses the role of IL-17E in promoting Th2 cell responses and the poorly defined functions of IL-17B, IL-17C, and IL-17D. The signaling mechanisms of IL-17RA are detailed, including its interaction with ACT1, a signaling adaptor, and its involvement in activating NF-κB, AP1, MAPK, and mRNA stability pathways. The article concludes by highlighting the potential therapeutic implications of understanding the IL-17R signaling pathways, particularly in the context of autoimmune diseases.The article provides an overview of the structure and signaling mechanisms of the IL-17 receptor superfamily, focusing on the unique features and functions of IL-17A and its receptor (IL-17RA). IL-17A, a hallmark cytokine of T helper 17 (T<H17) cells, plays a dual role in protecting against extracellular pathogens and promoting inflammatory pathology in autoimmune diseases. The IL-17R family, including IL-17RA and other receptor subunits, has distinct structural features and signaling pathways that differ from those of other cytokine subclasses. IL-17A and IL-17F, the best-characterized members of the IL-17 family, activate pro-inflammatory pathways through a novel ACT1-dependent pathway, leading to the activation of NF-κB, a key transcription factor associated with inflammation. The article also discusses the role of IL-17E in promoting Th2 cell responses and the poorly defined functions of IL-17B, IL-17C, and IL-17D. The signaling mechanisms of IL-17RA are detailed, including its interaction with ACT1, a signaling adaptor, and its involvement in activating NF-κB, AP1, MAPK, and mRNA stability pathways. The article concludes by highlighting the potential therapeutic implications of understanding the IL-17R signaling pathways, particularly in the context of autoimmune diseases.