The article discusses the role of T helper (Th) cells, particularly Th2 cells, in the pathogenesis of fibrotic diseases. It highlights the distinct mechanisms involved in inflammation and fibrosis, emphasizing that while inflammation is often a precursor to fibrosis, the severity of fibrosis does not always correlate with the intensity of inflammation. The author reviews experimental models that have been used to study fibrosis, such as those involving bleomycin and schistosomiasis, and discusses the importance of understanding the immunological mechanisms that regulate fibrogenesis. Key findings include: - Fibrosis is a significant cause of morbidity and mortality, affecting various tissues and organs. - Chronic inflammation, characterized by a large infiltrate of mononuclear cells, is crucial in the progression of fibrosis. - Th2 cells, which produce cytokines like IL-4, IL-5, and IL-13, play a central role in promoting fibrosis. - In contrast, Th1 cells, which produce interferon-γ (IFN-γ), have anti-fibrotic properties. - The balance between Th1 and Th2 responses is critical, with an imbalance leading to fibrosis. - IL-13, in particular, is a potent pro-fibrotic cytokine that can stimulate collagen production and fibroblast activation. - Chemokines, such as CCL3 and CCL2, are important regulators of fibrosis by recruiting macrophages and other effector cells. - Macrophages and fibroblasts are key effector cells in fibrosis, with macrophages differentiating into 'classically activated' (NOS2) or 'alternatively activated' (ARG1) phenotypes. - Regulatory T cells (TReg cells) and IL-10 have suppressive effects on fibrosis. - The IL-13 decoy receptor (sIL-13Rα2-Fc) is an effective inhibitor of IL-13 and can ameliorate fibrotic disease. The article concludes by suggesting that the Th2 response should be viewed as an adaptive tissue-healing mechanism rather than a simple counter-regulatory system to Th1 responses, and that targeting the fibrotic pathway with specific therapies may be a promising approach to treating fibrotic disorders.The article discusses the role of T helper (Th) cells, particularly Th2 cells, in the pathogenesis of fibrotic diseases. It highlights the distinct mechanisms involved in inflammation and fibrosis, emphasizing that while inflammation is often a precursor to fibrosis, the severity of fibrosis does not always correlate with the intensity of inflammation. The author reviews experimental models that have been used to study fibrosis, such as those involving bleomycin and schistosomiasis, and discusses the importance of understanding the immunological mechanisms that regulate fibrogenesis. Key findings include: - Fibrosis is a significant cause of morbidity and mortality, affecting various tissues and organs. - Chronic inflammation, characterized by a large infiltrate of mononuclear cells, is crucial in the progression of fibrosis. - Th2 cells, which produce cytokines like IL-4, IL-5, and IL-13, play a central role in promoting fibrosis. - In contrast, Th1 cells, which produce interferon-γ (IFN-γ), have anti-fibrotic properties. - The balance between Th1 and Th2 responses is critical, with an imbalance leading to fibrosis. - IL-13, in particular, is a potent pro-fibrotic cytokine that can stimulate collagen production and fibroblast activation. - Chemokines, such as CCL3 and CCL2, are important regulators of fibrosis by recruiting macrophages and other effector cells. - Macrophages and fibroblasts are key effector cells in fibrosis, with macrophages differentiating into 'classically activated' (NOS2) or 'alternatively activated' (ARG1) phenotypes. - Regulatory T cells (TReg cells) and IL-10 have suppressive effects on fibrosis. - The IL-13 decoy receptor (sIL-13Rα2-Fc) is an effective inhibitor of IL-13 and can ameliorate fibrotic disease. The article concludes by suggesting that the Th2 response should be viewed as an adaptive tissue-healing mechanism rather than a simple counter-regulatory system to Th1 responses, and that targeting the fibrotic pathway with specific therapies may be a promising approach to treating fibrotic disorders.