Immunological Adjuvance of Metabolic Origin: Oxidative Stress, Postulated Impaired Function of Thiol Proteases and Immunogenicity

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Abstract

Autoimmune disease may sometimes arise because of dysfunction of thiol proteases, which are vulnerable to oxidation of their sulphydryl groups. This may be initially signalled by hyperinsulinaemia, regarded here as a telltale phenomenon of oxidative stress and indicating difficulty in protein catabolism. Initial immunogenic sensitization may take place when antigen processing is altered by a metabolic process, which has locally overwhelmed the antioxidant systems and led to diminished thiol-protease digestion and to the repeated survival in critical cells of immunogenic peptide fragments. From this it follows than an immunological host may be either prejudiced towards or against tolerance by agents, respectively, which stabilize or destabilize antioxidant homeostasis.

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