**1. Introduction**

Autoimmune diseases occur when an individual develops an immune response targeted against specific organ or number of organs. Genetic susceptibility and environmental factors are the main responsible of the development of the autoimmune process leading to a clinically evident disease.

The majority of organ-specific autoimmune diseases are characterized by an initial infiltration by lymphocytes and macrophages, of the organ, with impaired activity of the organ followed by atrophy. This progressive autoimmune process takes time, and is T cell mediated. Antibodies against specific antigens of the involved gland are detectable in the blood before the clinical onset of the specific disease, so they represent a risk marker and their screening and follow-up allow precocious diagnosis and treatment of autoimmunerelated disease in genetically susceptible individuals (Allen et al., 2008).

Genetic factors and autoimmunity are closely related since the developmental maturation of T cells occurs through an interaction between HLA antigen and T cell receptor. In genetically susceptible individuals, disease-prone HLA molecules are ineffective at binding and presenting peptides from tissue-specific antigens, therefore auto-reactive T cells can survive and trigger a poorly regulated immune response thereafter (Van den Driessche, 2009).

Patients affected by type 1 diabetes mellitus are at increased risk of developing other autoimmune conditions like celiac disease, autoimmune thyroid disease, adrenal insufficiency, atrophic gastritis, autoimmune hepatitis, primary ovarian failure.

The frequency of organ specific autoimmunity in patients with type 1 diabetes might be due to multiple immunologic abnormalities, i.e an imbalance in B and T lymphocytes, or a tendency to react against specific antigens, or poor ability to develop immune tolerance.
