Genetic and molecular background in autoimmune diabetes mellitus

Česká verzia

Authors: D. Kantárová ^1,2; D. Prídavková ¹; I. Ságová ¹; M. Vrlík ²; J. Mikler ³; M. Buc ⁴
Authors place of work: I. interná klinika JLF UK a UNM, Martin, Slovensko ¹; Martinské centrum imunológie, Martin, Slovensko ²; Klinika detí a dorastu JLF UK a UNM, Martin, Slovensko ³; Imunologický ústav LF UK, Bratislava, Slovensko SÚHRN ⁴
Published in the journal: Epidemiol. Mikrobiol. Imunol. 64, 2015, č. 3, s. 121-129
Category: Review Article

Summary

Type 1 diabetes mellitus (T1 DM) is caused by autoimmune-mediated and idiopathic beta-cell destruction of the pancreatic islets of Langerhans resulting in absolute insulin deficiency. Susceptibility to T1 DM is influenced by both genetic and environmental factors. It is generally believed that in genetically susceptible individuals, the disease is triggered by environmental agents, such as viral infections, dietary factors in early infancy, or climatic influences. Many candidate genes for diabetes have been reported; those within the Major Histocompatibility Complex being among the most important. The most common autoantigens are insulin, glutamic acid decarboxylase 65, insuloma-associated antigen 2, and zinc transporter ZnT8. The destruction of b-cells is mediated mainly by cellular mechanisms; antibodies only seem to reflect the ongoing autoimmune processes and are not directly involved in the tissue damage. They, however, appear prior to the onset of insulin deficiency which makes them suitable for use in the prevention of the disease.

Keywords:
autoantigens – autoantibodies – HLA alleles – insuline – B, T, and NKT cells

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