Abstract
Type 1 diabetes mellitus is developing in a secondary way as a consequence of autoimmune destruction of b-cells of Langerhans pancreatic island. The heredity of type 1 diabetes has a polygenic character presented by a multiepistasis model where the predisposition to a immunopathological symptom is defined by a specific combination of multiple gene locuses and effects of environment.
The association of type 1 diabetes with certain human leucocyte antigens (HLA): DR3, DR4, DQB1*0201, DQB1*0302 and DQA1*0301 gives an evidence of the participation of HLA genetic marks in its ethiopathogenesis. The alleles of DQB1 gene are considered as the most important risk factor.
The absence of aspartic acid in codon 57 of DQB1 chain which takes part in the forming the immunogenetic epithope of the HLA molecule contributes significantly to the predisposition to the disease. It is presumed that predisposition HLA class II molecules present pathogenic peptides to CD-4 positive T lymphocytes.
Expression of such HLA-peptide complex on the surface of antigen presenting cells leads to initiation of autoimmune reactions of lymphocytes and inception of disease.