T-2 toxin, a trichothecene mycotoxin produced by Fusarium species, poses significant threats to poultry health and productivity. Contamination of feed with T-2 toxin leads to various pathological consequences, including damage to the gastrointestinal tract, liver, kidneys, and reproductive organs. It also impairs immune function by affecting the spleen, bursa of Fabricius, and thymus, leading to immunosuppression and increased susceptibility to infectious diseases. T-2 toxin induces oxidative stress and cellular damage through the production of reactive oxygen species and free radicals, contributing to apoptosis via activation of cellular signaling cascades. The toxin is metabolized primarily in the liver, with various metabolites such as HT-2 toxin being produced. Metabolic pathways involve hydrolysis, hydroxylation, sulfate conjugation, and de-epoxidation. The toxin's effects are influenced by factors such as the mode and frequency of exposure, dose, and the presence of other mycotoxins. T-2 toxin causes reduced feed intake, growth rate, and egg production, along with neurological and reproductive disorders. It also leads to oxidative stress, DNA damage, and apoptosis in various tissues, including the liver and spleen. The toxin affects the immune system by altering the balance of CD4+/CD8+ T cells and reducing antibody titers, which can impact vaccination effectiveness. T-2 toxin induces oxidative stress and mitochondrial dysfunction, leading to cellular damage and apoptosis. The toxin's effects are also linked to autophagy and endoplasmic reticulum stress. Overall, T-2 toxin has complex and multifaceted effects on poultry, necessitating strategies to mitigate its impact on avian health and food safety.T-2 toxin, a trichothecene mycotoxin produced by Fusarium species, poses significant threats to poultry health and productivity. Contamination of feed with T-2 toxin leads to various pathological consequences, including damage to the gastrointestinal tract, liver, kidneys, and reproductive organs. It also impairs immune function by affecting the spleen, bursa of Fabricius, and thymus, leading to immunosuppression and increased susceptibility to infectious diseases. T-2 toxin induces oxidative stress and cellular damage through the production of reactive oxygen species and free radicals, contributing to apoptosis via activation of cellular signaling cascades. The toxin is metabolized primarily in the liver, with various metabolites such as HT-2 toxin being produced. Metabolic pathways involve hydrolysis, hydroxylation, sulfate conjugation, and de-epoxidation. The toxin's effects are influenced by factors such as the mode and frequency of exposure, dose, and the presence of other mycotoxins. T-2 toxin causes reduced feed intake, growth rate, and egg production, along with neurological and reproductive disorders. It also leads to oxidative stress, DNA damage, and apoptosis in various tissues, including the liver and spleen. The toxin affects the immune system by altering the balance of CD4+/CD8+ T cells and reducing antibody titers, which can impact vaccination effectiveness. T-2 toxin induces oxidative stress and mitochondrial dysfunction, leading to cellular damage and apoptosis. The toxin's effects are also linked to autophagy and endoplasmic reticulum stress. Overall, T-2 toxin has complex and multifaceted effects on poultry, necessitating strategies to mitigate its impact on avian health and food safety.