The article discusses the role of complement bypass systems in human diseases and the importance of more specific and quantitative assays for detecting complement activity. It highlights that these bypass pathways are often overlooked in studies examining the complement system's role in disease, emphasizing the need to consider them in clinical and animal models. The article also provides a cautionary note about the limitations of using C4-deficient animals to rule out the classical or lectin pathways in mouse models of human diseases, as bypass cascades can still operate in these "deficient" states. The second part of the article focuses on the IL-23/IL-17 axis in inflammation. It explains how IL-23 induces the differentiation of naive CD4+ T cells into Th17/Th17 cells, which produce IL-17, IL-6, and TNF-α. Studies show that blocking IL-23 or its downstream factors, particularly IL-17 and IL-6, can significantly suppress disease development in models of inflammatory bowel disease and multiple sclerosis. The article discusses the mechanisms by which IL-23 promotes the development of Th17/Th17 cells and how this axis is critical for the development of autoimmune inflammatory diseases. It also explores the role of IL-23 in host defense against bacterial infections and the involvement of additional factors in the differentiation of Th17/Th17 cells. The article concludes by emphasizing the importance of understanding the distinct pathways involved in inflammatory responses and the potential therapeutic targets for autoimmune and allergic inflammatory diseases.The article discusses the role of complement bypass systems in human diseases and the importance of more specific and quantitative assays for detecting complement activity. It highlights that these bypass pathways are often overlooked in studies examining the complement system's role in disease, emphasizing the need to consider them in clinical and animal models. The article also provides a cautionary note about the limitations of using C4-deficient animals to rule out the classical or lectin pathways in mouse models of human diseases, as bypass cascades can still operate in these "deficient" states. The second part of the article focuses on the IL-23/IL-17 axis in inflammation. It explains how IL-23 induces the differentiation of naive CD4+ T cells into Th17/Th17 cells, which produce IL-17, IL-6, and TNF-α. Studies show that blocking IL-23 or its downstream factors, particularly IL-17 and IL-6, can significantly suppress disease development in models of inflammatory bowel disease and multiple sclerosis. The article discusses the mechanisms by which IL-23 promotes the development of Th17/Th17 cells and how this axis is critical for the development of autoimmune inflammatory diseases. It also explores the role of IL-23 in host defense against bacterial infections and the involvement of additional factors in the differentiation of Th17/Th17 cells. The article concludes by emphasizing the importance of understanding the distinct pathways involved in inflammatory responses and the potential therapeutic targets for autoimmune and allergic inflammatory diseases.