Abstract
Regulatory T cells (Tregs) are essential for limiting immunopathology and maintaining immune homeostasis. They represent a major barrier to aberrant and excessive immune responses to pathogens and allergens in infectious and allergic diseases, respectively. In this review, we describe our current understanding of the immunopathogenic mechanism behind protection against the development and exacerbation of severe drug eruptions, with special emphasis on regulatory T cells (Tregs). In this regard, our previous study demonstrated that the timing of the dysfunction of Tregs could determine the pathological phenotype and sequelae of severe drug eruptions. We also discuss the factors that abrogate Treg function and demonstrate that Mycoplasma pneumoniae is the only pathogen shown to cause a persistent loss of Treg function long after clinical resolution. A loss of Treg function observed at the different stages of severe drug eruptions would be a driving force in the subsequent development of autoimmune disease as long-term sequelae of severe drug eruptions.
Keywords: Drug-induced hypersensitivity syndrome, fixed drug eruption, herpesviruses, Mycoplasma pneumoniae, regulatory T cells, Stevens-Johnson syndrome, toxic epidermal necrolysis.
Graphical Abstract
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