The article reviews the emerging data on the role of T helper (TH)17 cells in host defense against specific pathogens and their involvement in autoimmunity and tissue inflammation. TH17 cells, characterized by the production of IL-17A, IL-17F, and IL-22, are induced by IL-6 and transforming growth factor-β (TGF-β). These cells play a crucial role in clearing extracellular pathogens not effectively handled by TH1 or TH2 cells. The differentiation of TH17 cells is independent of the transcription factors involved in TH1 or TH2 differentiation. Instead, STAT3 and ROR-γt are critical for TH17 differentiation. IL-21, produced by TH17 cells, amplifies the TH17 response, while IL-23 stabilizes the TH17 phenotype. The reciprocal relationship between TH17 and regulatory T (Treg) cells is also discussed, with TGF-β inducing FOXP3 expression in Treg cells and IL-6 inhibiting Treg cell generation while inducing TH17 cells. Several cytokines and pathways, such as IL-4, IL-25, IFN-γ, IL-27, and retinoic acid, can inhibit TH17 cell development and expansion. The article concludes by proposing a three-step model for TH17 cell differentiation: induction, amplification, and maintenance/stabilization, highlighting the importance of these steps in understanding TH17 cell function and potential therapeutic targets.The article reviews the emerging data on the role of T helper (TH)17 cells in host defense against specific pathogens and their involvement in autoimmunity and tissue inflammation. TH17 cells, characterized by the production of IL-17A, IL-17F, and IL-22, are induced by IL-6 and transforming growth factor-β (TGF-β). These cells play a crucial role in clearing extracellular pathogens not effectively handled by TH1 or TH2 cells. The differentiation of TH17 cells is independent of the transcription factors involved in TH1 or TH2 differentiation. Instead, STAT3 and ROR-γt are critical for TH17 differentiation. IL-21, produced by TH17 cells, amplifies the TH17 response, while IL-23 stabilizes the TH17 phenotype. The reciprocal relationship between TH17 and regulatory T (Treg) cells is also discussed, with TGF-β inducing FOXP3 expression in Treg cells and IL-6 inhibiting Treg cell generation while inducing TH17 cells. Several cytokines and pathways, such as IL-4, IL-25, IFN-γ, IL-27, and retinoic acid, can inhibit TH17 cell development and expansion. The article concludes by proposing a three-step model for TH17 cell differentiation: induction, amplification, and maintenance/stabilization, highlighting the importance of these steps in understanding TH17 cell function and potential therapeutic targets.