Abstract
Type 1 diabetes (T1D) is an autoimmune disease triggered by environmental factors. Among those of infectious origin, viruses mostly associated to T1D are rubella virus, enteroviruses (Rotavirus, Coxackie B), Cytomegalovirus and mumps virus. The role of bacterial infections is still controversial, acting either as modulators or precipitating factors of an already started autoimmune process. Polymorphic genes of innate immunity, such as Toll-like receptors, nucleotide-binding oligomerization domain (NOD) 1 and NOD2 and mannose-binding lectin (MBL) genes, did not show a strict association with T1D onset, while protein tyrosine phosphatase (PTPN22), cytotoxic T-lymphocyte antigen (CTLA)4 and natural killer cells immunoglobulin-like receptor (KIR) genes appear to play an important role. However, the adaptive immune response genes (HLA) still provide the major contribution to T1D susceptibility. Here, we review the mechanism by which microorganisms might induce autoimmunity.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
The authors thank Natascia Bordino and Niccolò Lanati for their contribution in the revision of the literature and English text, and Miss Marisa Scottini for editing the text and figure of this review.