Discuss the current knowledge of the contribution of cellular and molecular components of the immune system to the pathology of type 1 diabetes
An autoimmune disease resulting in insulin deficiency, Type 1 diabetes mellitus. There have been countless studies into its causes; there is still no solid answer. Previous studies strongly implicated Th1 cells to play a key role in the progression of type 1 diabetes, however, recent studies have been showing that this is inadequate to explain the pathology of the autoimmune disease Type 1 diabetes. In fact other constituents of the immune system are accountable; Th17 cells play a huge role in the cellular pathology of Type 1 diabetes.
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Glutamic acid decarboxylase (GADA), insulinoma-associated autoantigen 2 (IA2A), and zinc transporter 8 (ZnT8A) are autoantibodies that have been found to be involved in this development (Atkins et al. 2014). There have been several recent studies that have led to the discovery of the roles of Th1 and Th17 in the pathology of Type 1 diabetes. Both of these T helper cells produce cytokines which lead to inflammation, these have always been thought to protect the body, however recent studies have shown that inflammation leads to autoimmunity rather than defence. There are specific cytokines produced by Th17 which have been found to especially bring about inflammation, IL-17A and IL-17F (Grunnet & Poulson 2011). Studies have found that restriction of Th17 has considerably hindered the progress of type 1 diabetes, further showing that Th17 cells are involved in the pathology of T1D. The roles Th17 plays in the pathology of type 1 diabetes were previously associated with Th1 cells before recent studies started suggesting otherwise. Current studies establish that inhibition of Th17 cells can influence the course of Type 1 diabetes. CD8+ T cells are activated by IL-2, which is a cytokine produced by Th1 cells these differentiate into cytotoxic T cells and are moved into the islets of Langerhans and are involved in the destruction of insulin producing beta- cells. (Ji-Won. Y., Jun. H., 2005)
Inflammation is a considerable factor in the development of type 1 diabetes, it has a lot of involvement in the damage of cells of the islets of Langerhans, there have been many studies showing that inflammation is a lot more present in T1D patients than in people who are not patients. Extreme inflammation has been found to play a major role in the loss of and the damage of beta cells. This specific kind of inflammation is called Insulitis, it is characterised by the access of harmful T cells into the pancreatic cells.
There are many antigen-presenting cells involved in the pathogenesis of type 1 diabetes, the dendritic cell is a key antigen presenting cell, it is different as it fuels T cells. Dendritic cells are the first cells that reach the islets of Langerhans, even before any T helper cells. Studies have shown that dendritic cells have some control in the regulation of pancreatic autoimmune responses. When the dendritic cells o the cell membrane are recognised by T helper cells and a major histocompatibility complex (MHC) is formed. Type 1 diabetes is characterised by leucocyte entry into pancreatic cells and then followed by immune destruction of insulin producing beta cells in the islets. CD4 AND CD8 T cells have major key roles as antigen presenting cells in the autoimmune response of the immune system (Jansen et al. 1995). An increased number of antigen presenting cells is required for the generation of tolerance, not immunisation, dendritic cells may be the activation behind regulatory T cells. The pathology of chronic type 1 diabetes has many...