The IL-23-IL-17 immune axis has been a major focus of immunological research, revealing key insights into T helper cell (Th17) development, function, and role in immune-mediated inflammatory diseases. Th17 cells, characterized by their production of IL-17 and IL-22, are critical in host defense and autoimmune pathogenesis. The discovery of IL-23 and its role in Th17 cell differentiation has transformed our understanding of cellular immunity. IL-23, along with IL-17, plays a central role in the pathogenesis of diseases such as psoriasis, multiple sclerosis, Crohn's disease, and ankylosing spondylitis. Anti-IL-17 and anti-IL-23 therapies have shown remarkable efficacy in treating these conditions. Th17 cells are regulated by a complex network of transcription factors, including RORγt, STAT3, IRF4, and BATF, which control their differentiation, stability, and plasticity. IL-6, IL-1β, and TGFβ are essential for Th17 development, while IL-23 is crucial for their pathogenicity. The interplay between these cytokines and transcription factors determines the balance between protective and autoimmune functions of Th17 cells. IL-23 enhances Th17 cell function by upregulating IL-23R and promoting the expression of pro-inflammatory cytokines. Recent studies have highlighted the importance of epigenetic modifications in Th17 cell plasticity and stability. The transcriptional control of Th17 cells involves intricate interactions between transcription factors and chromatin remodeling. The IL-17 receptor (IL-17R) and its signaling pathways are critical for mediating the effects of IL-17, which includes the induction of chemokines, antimicrobial peptides, and inflammatory responses. However, dysregulated IL-17 signaling can lead to autoimmune diseases, and negative regulatory mechanisms, such as deubiquitination and proteasomal degradation, help to control its activity. Th17 cells are involved in both host defense and autoimmune diseases. While they provide protection against pathogens, their overactivation can lead to chronic inflammation and tissue damage. The development of targeted therapies against IL-17 and IL-23 has shown promising results in treating inflammatory diseases. However, the complexity of the IL-23-IL-17 axis and the potential for off-target effects require further investigation. Understanding the molecular mechanisms underlying Th17 cell function and regulation is essential for developing more effective and safer therapeutic strategies.The IL-23-IL-17 immune axis has been a major focus of immunological research, revealing key insights into T helper cell (Th17) development, function, and role in immune-mediated inflammatory diseases. Th17 cells, characterized by their production of IL-17 and IL-22, are critical in host defense and autoimmune pathogenesis. The discovery of IL-23 and its role in Th17 cell differentiation has transformed our understanding of cellular immunity. IL-23, along with IL-17, plays a central role in the pathogenesis of diseases such as psoriasis, multiple sclerosis, Crohn's disease, and ankylosing spondylitis. Anti-IL-17 and anti-IL-23 therapies have shown remarkable efficacy in treating these conditions. Th17 cells are regulated by a complex network of transcription factors, including RORγt, STAT3, IRF4, and BATF, which control their differentiation, stability, and plasticity. IL-6, IL-1β, and TGFβ are essential for Th17 development, while IL-23 is crucial for their pathogenicity. The interplay between these cytokines and transcription factors determines the balance between protective and autoimmune functions of Th17 cells. IL-23 enhances Th17 cell function by upregulating IL-23R and promoting the expression of pro-inflammatory cytokines. Recent studies have highlighted the importance of epigenetic modifications in Th17 cell plasticity and stability. The transcriptional control of Th17 cells involves intricate interactions between transcription factors and chromatin remodeling. The IL-17 receptor (IL-17R) and its signaling pathways are critical for mediating the effects of IL-17, which includes the induction of chemokines, antimicrobial peptides, and inflammatory responses. However, dysregulated IL-17 signaling can lead to autoimmune diseases, and negative regulatory mechanisms, such as deubiquitination and proteasomal degradation, help to control its activity. Th17 cells are involved in both host defense and autoimmune diseases. While they provide protection against pathogens, their overactivation can lead to chronic inflammation and tissue damage. The development of targeted therapies against IL-17 and IL-23 has shown promising results in treating inflammatory diseases. However, the complexity of the IL-23-IL-17 axis and the potential for off-target effects require further investigation. Understanding the molecular mechanisms underlying Th17 cell function and regulation is essential for developing more effective and safer therapeutic strategies.