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• W1484211092 abstract "Type 1 diabetes, formerly termed insulin-dependent diabetes mellitus (IDDM), is a chronic organ-specific autoimmune disorder thought to be caused by proinflammatory autoreactive CD4+ and CD8+ T cells, which mediate progressive and selective damage of insulinproducing pancreatic beta-cells (Atkinson & Eisenbarth, 2001). The reduction of beta-cell mass leads to a lack of insulin and thereby loss of blood glucose control (Boettler & von Herrath, 2010). The worldwide prevalence of T1D was estimated to be 171 million cases among the adult population (Wild et al., 2004). Its annual incidence varies widely from one country to another (from less than 1 per 100,000 inhabitants in Asia to approximately up to 25/100,000 population/year in North America, more than 30 per 100,000 in Scandinavia and up to 41/100,000 population/year in Europe). It is in steady increase across the globe, especially among children aged less than five years (Kajander et al., 2000; Vija et al., 2009). According to the European Diabetes (EURODIAB) study group, the prevalence of T1D in Europe will increase significantly in children younger than 15 years of age to reach 160,000 cases in 2020 (Patterson et al., 2009). These data will result in an increasing number of patients with longstanding diabetes and with a risk of serious complications (Kessler, 2010). These include heart diseases and strokes, high blood pressure, renal failure and ketoacidosis (DKA) (Boettler & von Herrath, 2010). To date, it has not been possible to prevent the autoimmune response to beta-cells in human, due probably to its unknown aetiology, although it is known that development of T1D is genetically controlled and thought to be initiated in susceptible individuals by environmental factors such as virus infections (Luo et al., 2010; Mukherjee & DiLorenzo, 2010; von Herrath, 2009). It is now evident that targeted destruction may go undetected for many years, but antibodies to various beta-cell antigens can be easily demonstrable in the sera of patients at risk before clinical onset (Achenbach et al., 2005). Additionally, some endogenous insulin secretion is generally present at the onset of clinical diabetes (Scheen, 2004), during which time, immunotherapeutic intervention may be effective (Staeva-Vieira et al., 2007). This chapter emphasizes the principal immunological risk markers of T1D and especially the role of cell-mediated immune response leading to pancreatic beta-cells destruction, as well as the most promising immunotherapeutic approaches for prevention and treatment of the disease." @default.
• W1484211092 created "2016-06-24" @default.
• W1484211092 creator A5046980798 @default.
• W1484211092 date "2011-11-25" @default.
• W1484211092 modified "2023-10-04" @default.
• W1484211092 title "Autoimmunity and Immunotherapy of Type 1 Diabetes" @default.
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