Rubella and autoimmunity.

303 Rev Bras Reumatol 2012;52(3):303-306 Molecular mimicry has been proposed as a pathogenic mechanism for autoimmune disease. The hypothesis is based on the epidemiological, clinical, and experimental studies and in evidence fi nding an association between infectious agents and autoimmune disease, observing cross-reactivity of immune agents with host antigens and microbial determinants.1 Recent studies have revealed that carbohydrate mimicry of bacterial lipo-oligosaccharide by the human ganglioside is an important cause of Guillain-Barré syndrome, for example. This new concept that carbohydrate mimicry can cause an autoimmune disease provides a clue of the pathogenesis of immune-mediated diseases.1 Molecular mimicry is based on a structural similarity between a pathogen or metabolite and self-structure. The similarity could be expressed as shared amino acid sequences or as a similar conformational structure between a pathogen and self-antigen.2 The strongest association of viruses and type 1 diabetes (T1D) involves enterovirus species, of which some strains have the ability to induce or accelerate autoimmune disease in animal models. Several hypotheses regarding the mechanism to explain how viruses affect islet autoimmunity and beta-cell destruction were proposed.3 Viral infection may serve as an accelerating factor that, superimposed onto advanced insulinitis, leads to rapid culmination into hyperglycemia. Rubella virus is a possible environmental agent which may be involved in the triggering of autoimmunity to pancreatic islet cells, leading to T1D. Autoantibody responses were found in 239 10-year-old girls who received live attenuated rubella vaccine, of whom 61 (26%) had no pre-existing rubella immunity.4 Infection can promote the expression of human endogenous retroviruses by molecular mimicry or by functional mimicry.5 There are additional mechanisms which may control the expression of human endogenous retroviruses, such as the epigenetic status of the genome.6 T1D develops during months to years, in which islet autoimmunity destroys the insulin-producing beta cells of the pancreas. This period is marked by the presence of antibodies Rubella and autoimmunity