Affiliation:
1. Università di Pavia, Dipartimento di Medicina Preventiva Occupazionale e di Comunità, Sezione di Igiene, Via Forlanini 2-27100 Pavia, Italy.
2. Fondazione IRCCS, Laboratorio di Immunogenetica, Servizio di Immunoematologia e Medicina Trasfusionale, Policlinico S. MatteoViale Golgi, 19-27100 Pavia, Italy.
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.
Subject
Pediatrics,Pediatrics, Perinatology, and Child Health
Cited by
1 articles.
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