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Response of Immune System in Type 1 Diabetes Patients

Kulvinder Kaur

Immune systems are documented as suppressors of immunity. Thus decrease in GM loss of control of immune system -followed by immune cell actions against cells of self,-ultimately T1D. Correlation of early fruit introduction relates to increase in autoimmunity to β-cells .Possibly abnormal immune response to solid food antigens in immature gut immune system in children that possess HLA susceptibility to DM. Moreover over load hypothesis points that environmental food exposures might over stimulate β- cell =>increased autoimmune mediated damage. Similarly increased amounts of bovine milk products increased risk of autoimmunity in children that possess HLA susceptibility. This might be due to insulin auto antibody in view of cross reactivity between bovine as well as human insulin. Gluten foods(cereals) in children <3yrs significant increase in islet autoantibody synthesis .DM patients with HLA-DR allele have increased Tcell reactivity to gluten derived polypeptides .This is secondary to interferonÆ´ ( IFNÆ´) as well as IL-17 liberation .Intestinal inflammation as well as T cell activation induced by gluten => β-cell autoimmunity. Vit D can modify T as well as Bcells function. VDR agonists => Treg cell induction. By stimulation of tolerance as well as stop differentiation as well as maturation of DC’s, downregulate expression of costimulatory molecules like CD40, CD80 and CD 86 and decrease IL-10 production,Viruses might => T1D by 2 modes )a direct cytolytic action on β-cells(like ds RNA virus-fig1) or ii)Indirect triggering of a DM –related autoimmune process against β-cells that=> β-cells destruction.