An autoimmune disease (AD) occurs in a situation where an individual's protective immune system attacks and destroys the individual's own tissues and organ(s), causing a recognizable syndrome(s). The viruses feature in the triggering of autoimmune diseases in genetically primed individuals through generating a viral group of regulatory immediate early proteins (IE). The IE indulges in promiscuous regulations of the viral replications as well as of host intracellular proteins. But there are consequences in the IE controlling host cell protein regulations, which we suggest as: the IE titration of the transactivator protein, autoimmune regulator (AIRE), which causes abolition of central tolerance; and the IE titration of the repressor protein, FOXP3, which results in the breach of peripheral tolerance. Titrations of AIRE and FOXP3 allow the escape of autoreactive T cells into the (peripheral) circulation where they can reach and zero in on self-tissues. The AD-predisposing MHC-II-DR-DQ haplotypes probably play a crucial role in the shaping of the T cell repertoire intrathymically for the survival of budding autoreactive T cell receptors (TCRs). Finally, we suggest there is IE titration of the repressors, the histone deacetylases (HDACs), in target organ cells which then consequentially express de novo MHC-II molecules and become de novo non-professional antigen-presenting cells (APCs), able to present viral peptides to cognate TCRs, thereby enrolling themselves for apoptotic death: a destiny of all APCs in immune responses, in general. Extensive apoptotic destruction of organ cells leads to an autoimmune syndrome(s).
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