This review article comprehensively analyzes the pathological consequences, metabolism, and toxic effects of T-2 toxin in poultry. T-2 toxin, a potent trichotheccene mycotoxin produced primarily by *Fusarium* species, poses a significant threat to animal health and productivity in livestock production, particularly in poultry. The toxin exhibits a broad spectrum of negative effects, including gastrointestinal tract damage, liver and kidney impairment, and reproductive disorders. It also severely impacts the immune system, leading to immunosuppression and increased susceptibility to infectious diseases. The toxin's metabolism in poultry is primarily mediated by the liver, with 19 different metabolites detected in feces and bile. The major metabolic pathways involve hydrolysis, hydroxylation, carboxylation, and sulfation. T-2 toxin induces apoptosis through various cellular signaling cascades and causes oxidative stress by increasing reactive oxygen species (ROS) production. The review highlights the importance of understanding these effects to develop strategies for mitigating the impact of T-2 toxin on avian health and food safety. Key findings include the significant economic losses due to T-2 toxin contamination, the need for comprehensive meteorological surveillance and strict quality control measures, and the potential synergistic effects of co-occurring mycotoxins. The article also discusses the immunomodulatory effects of T-2 toxin, its genotoxicity, and the detailed mechanism of action, including the disruption of DNA, RNA, and protein synthesis. Finally, the review emphasizes the oxidative stress-induced cytotoxicity and apoptosis, providing insights into the underlying mechanisms and potential protective strategies.This review article comprehensively analyzes the pathological consequences, metabolism, and toxic effects of T-2 toxin in poultry. T-2 toxin, a potent trichotheccene mycotoxin produced primarily by *Fusarium* species, poses a significant threat to animal health and productivity in livestock production, particularly in poultry. The toxin exhibits a broad spectrum of negative effects, including gastrointestinal tract damage, liver and kidney impairment, and reproductive disorders. It also severely impacts the immune system, leading to immunosuppression and increased susceptibility to infectious diseases. The toxin's metabolism in poultry is primarily mediated by the liver, with 19 different metabolites detected in feces and bile. The major metabolic pathways involve hydrolysis, hydroxylation, carboxylation, and sulfation. T-2 toxin induces apoptosis through various cellular signaling cascades and causes oxidative stress by increasing reactive oxygen species (ROS) production. The review highlights the importance of understanding these effects to develop strategies for mitigating the impact of T-2 toxin on avian health and food safety. Key findings include the significant economic losses due to T-2 toxin contamination, the need for comprehensive meteorological surveillance and strict quality control measures, and the potential synergistic effects of co-occurring mycotoxins. The article also discusses the immunomodulatory effects of T-2 toxin, its genotoxicity, and the detailed mechanism of action, including the disruption of DNA, RNA, and protein synthesis. Finally, the review emphasizes the oxidative stress-induced cytotoxicity and apoptosis, providing insights into the underlying mechanisms and potential protective strategies.