Abstract
Type 1diabetes (T1D) is an autoimmune disease commonly observed in the young population and characterized by the destruction of pancreatic beta-cells. Defective self and non-self-recognition in collaborative functioning of the innate and adaptive immune system lead to the pathogenesis of T1D. The present review brings to light the components of innate immunity like macrophages, Toll-like receptors (TLR), viral components in prompting T1D. Macrophages mediate beta-cell cytotoxicity and cause inflammatory response; TLRs trigger the release of various cytokines and activate adaptive immune response; viruses mimic their components as ligands to initiate TLR signaling and therefore contribute to T1D pathogenesis. Both humoral and cellular components of adaptive immune responses are involved in the development of T1D. In humoral autoimmunity, the presence of different autoantibodies that detect respective beta-cells autoantigens can start to damage pancreatic beta-cells. The appearance of a particular autoantibody at onset age is considered as a diagnostic marker. The cellular response attributes mainly in T1D pathogenesis, with the help of CD4+ and CD8+T cells CD4+T cells release cytokines and mediate phagocytosis, it also stimulates B cells for antibody production thus cognating humoral and cellular autoimmune response. CD8+Tcells generate direct cytotoxicity to beta-cells when MHC (Major histocompatibility complex) II molecules present antigenic peptides.