Tissue fibrosis, a leading cause of morbidity and mortality, is a complex process involving the replacement of normal tissue with connective tissue. Current treatments for fibrotic diseases, such as idiopathic pulmonary fibrosis, hepatic fibrosis, and systemic sclerosis, target inflammatory pathways but have been largely ineffective due to the distinct mechanisms of fibrogenesis compared to inflammation. Experimental models, including those using bleomycin, have helped elucidate the molecular mechanisms of fibrosis. Fibrosis is a pathological response to chronic injury, often involving adaptive immune responses, particularly T helper 2 (T_H2) cells, which produce cytokines like IL-4, IL-5, and IL-13. These cytokines promote fibrosis by stimulating collagen synthesis and tissue remodeling. In contrast, T_H1 cells, which produce IFN-γ, can suppress fibrosis. The balance between T_H1 and T_H2 responses is crucial in fibrogenesis. IL-13, in particular, plays a significant role in fibrosis by activating pathways that lead to collagen deposition and tissue scarring. Studies have shown that IL-13 can induce fibrosis independently of TGF-β, highlighting its importance in fibrogenesis. The role of macrophages and fibroblasts in fibrosis is also critical, with macrophages differentiating into functionally distinct populations based on cytokine exposure. Regulatory T cells and IL-10 have been shown to suppress fibrosis by modulating immune responses and reducing collagen synthesis. The development of antifibrotic therapies, including IL-13 inhibitors and TGF-β antagonists, is an active area of research. These therapies aim to target the underlying mechanisms of fibrosis, such as the activation of fibroblasts and the production of pro-fibrotic cytokines, to prevent or reverse fibrotic disease. Understanding the complex interplay between immune responses and fibrosis is essential for developing effective treatments.Tissue fibrosis, a leading cause of morbidity and mortality, is a complex process involving the replacement of normal tissue with connective tissue. Current treatments for fibrotic diseases, such as idiopathic pulmonary fibrosis, hepatic fibrosis, and systemic sclerosis, target inflammatory pathways but have been largely ineffective due to the distinct mechanisms of fibrogenesis compared to inflammation. Experimental models, including those using bleomycin, have helped elucidate the molecular mechanisms of fibrosis. Fibrosis is a pathological response to chronic injury, often involving adaptive immune responses, particularly T helper 2 (T_H2) cells, which produce cytokines like IL-4, IL-5, and IL-13. These cytokines promote fibrosis by stimulating collagen synthesis and tissue remodeling. In contrast, T_H1 cells, which produce IFN-γ, can suppress fibrosis. The balance between T_H1 and T_H2 responses is crucial in fibrogenesis. IL-13, in particular, plays a significant role in fibrosis by activating pathways that lead to collagen deposition and tissue scarring. Studies have shown that IL-13 can induce fibrosis independently of TGF-β, highlighting its importance in fibrogenesis. The role of macrophages and fibroblasts in fibrosis is also critical, with macrophages differentiating into functionally distinct populations based on cytokine exposure. Regulatory T cells and IL-10 have been shown to suppress fibrosis by modulating immune responses and reducing collagen synthesis. The development of antifibrotic therapies, including IL-13 inhibitors and TGF-β antagonists, is an active area of research. These therapies aim to target the underlying mechanisms of fibrosis, such as the activation of fibroblasts and the production of pro-fibrotic cytokines, to prevent or reverse fibrotic disease. Understanding the complex interplay between immune responses and fibrosis is essential for developing effective treatments.