T-cell recognition of lipid peroxidation products breaks tolerance to self proteins

摘要: Peroxidation of polyunsaturated fatty acids in lipoproteins and cell membrane phospholipids occurs many situations the body, both under normal pathological conditions. Low-density lipoprotein is particularly prone to oxidation believed be a pathogenetic component atherogenesis. Both antibody responses T-cell oxidatively modified have been demonstrated humans as well animal models. However, little known about how these arise or T cells recognize antigens. In present study, mice were immunized with homologous albumin covalently series defined aldehydes which are generated during lipid peroxidation. hybridomas from animals major histocompatibility complex-restricted protein sequence-dependent albumin, but not native albumin. addition response epitopes, some aldehyde modifications resulted strong also non-modified protein. This T-cell-dependent break tolerance constitutes novel pathway for induction autoimmunity by The findings implications where peroxidation products generated, including atherosclerosis inflammatory infectious diseases.