Mouat Isobel C, Morse Zachary J, Jean-Baptiste Virginie S E, Allanach Jessica R, Horwitz Marc S
Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada.
Front Endocrinol (Lausanne). 2017 Sep 19;8:238. doi: 10.3389/fendo.2017.00238. eCollection 2017.
The first Fresh Ideas, Foundational Experiments (FIFE): Immunology and Diabetes symposia workshop took place in 2016 and exemplified the active interest of a number of several investigators interested the global rise in the incidence of type 1 diabetes (T1D). This increase does not correlate with genetic drift and indicates that environmental exposures are playing an increasingly significant role. Despite major biomedical and technological advances in diagnosis and treatment, treatments are frequently insufficient as they do not inhibit the progression of the underlying autoimmune response and often fail to prevent life-threatening complications. T1D is the result of autoimmune destruction of the insulin-producing beta cells of the pancreas, and the precise, mechanistic contribution of the immune system to disease pathogenesis and progression remains to be fully characterized. Ultimately, the combinatorial effect of concurrent factors, including beta cell fragility, exogenous stressors, and genetic priming of the innate and adaptive immune system, work together to induce T1D autoimmunity. Thus, T1D is the result of immunological defects and environmental pathogens, requiring the sustained attention of collaborative research teams such as FIFE: I & D with varied perspectives, unified by the universally held goal of finding a sustainable, life-long cure. Herein, the authors provide perspective on various fields in T1D research highlighted by speakers participating in the inaugural FIFE symposium.
首届“新观点、基础实验(FIFE):免疫学与糖尿病”研讨会于2016年举行,体现了众多研究人员对1型糖尿病(T1D)全球发病率上升的积极关注。这种增加与基因漂移无关,表明环境暴露正在发挥越来越重要的作用。尽管在诊断和治疗方面取得了重大的生物医学和技术进步,但治疗往往并不充分,因为它们无法抑制潜在的自身免疫反应的进展,而且常常无法预防危及生命的并发症。T1D是胰腺中产生胰岛素的β细胞发生自身免疫破坏的结果,免疫系统对疾病发病机制和进展的确切、机制性贡献仍有待充分阐明。最终,包括β细胞脆弱性、外源性应激源以及先天和适应性免疫系统的基因启动等并发因素的综合作用共同导致了T1D自身免疫。因此,T1D是免疫缺陷和环境病原体的结果,需要像FIFE:免疫学与糖尿病这样具有不同视角的合作研究团队持续关注,这些团队因寻找可持续的终身治愈方法这一共同目标而团结在一起。在此,作者提供了参与首届FIFE研讨会的演讲者所强调的T1D研究各个领域的观点。