TYPE 2 DIABETES MELLITUS – AN AUTOIMMUNE DISEASE?

Abstract

In recent years, the association of type 2 diabetes mellitus (DM) to autoimmune diseases has been discussed. Participation of innate immunity in the development of inflammation in obesity and insulin resistance, which determine the development of type 2 DM is well known. These changes, along with gluco-and lipotoxicity, lead to the destruction of the pancreatic β cells, emergence of autoantigens and development both humoral and cell type autoimmune reactions. The effectiveness of drugs used in the treatment of autoimmune diseases also leads some authors to the conclusion that type 2 diabetes can be referred to autoimmune diseases. However, most researchers believe that the presence of an autoimmune component is a side effect of inflammation and do not consider type 2 diabetes as an autoimmune disease. Alternatively, autoimmune reactions may take part in the pathogenesis of type 2 diabetes because: a viral infection contributes to the development of antiviral immunity, however, in the presence of in-sulin-cross-reactive antigens, an autoimmune reaction is observed. Most patients with uncompromised immune system, the clone of auto-aggressive cells sensitized to insulin is destroyed. In a small percent-age of patients with impaired immune system, insulin-sensitized lymphocytes do not die that leads to destruction of pancreatic islet cells and development of type 1 diabetes. In other patients, on the one hand, the immune system is also unable to remove the cell clone exerting signs of autoaggression, but it tries to suppress this effect by blocking insulin receptors on immunocompetent cells. This maneuver succeeds, and suppression is reversible. However, insulin receptors are abundant not only on sensitized lymphocytes, but also on liver cells, muscles, and adipose tissue. The effect of blocking insulin receptors in insulin-sensitive tissues contributes to the development of primary insulin resistance, which precedes and contributes to the development of obesity. Subsequently, excessive intake of dietary fats results in obesity progression, so that the entire cascade of inflammatory reactions is involved in the pathological process. This, in turn, contributes to the formation of secondary insulin resistance, which accounts for the development of type 2 diabetes and cardiovascular diseases and so on. Type 2 diabetes does not belong to autoimmune diseases, but suppressed autoimmune reactions with respect to insulin play a role in the development of insulin resistance.