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Islet inflammation in type 2 diabetes

Published on Jul 1, 2019in Seminars in Immunopathology6.804
· DOI :10.1007/s00281-019-00745-4
Marianne Böni-Schnetzler2
Estimated H-index: 2
(University Hospital of Basel),
Daniel T. Meier1
Estimated H-index: 1
(University Hospital of Basel)
Abstract
Metabolic diseases including type 2 diabetes are associated with meta-inflammation. β-Cell failure is a major component of the pathogenesis of type 2 diabetes. It is now well established that increased numbers of innate immune cells, cytokines, and chemokines have detrimental effects on islets in these chronic conditions. Recently, evidence emerged which points to initially adaptive and restorative functions of inflammatory factors and immune cells in metabolism. In the following review, we provide an overview on the features of islet inflammation in diabetes and models of prediabetes. We separately emphasize what is known on islet inflammation in humans and focus on in vivo animal models and how they are used to elucidate mechanistic aspects of islet inflammation. Further, we discuss the recently emerging physiologic signaling role of cytokines during adaptation and normal function of islet cells.
  • References (108)
  • Citations (2)
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References108
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#2Klaus H. Kaestner (UPenn: University of Pennsylvania)H-Index: 91
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#2Yun Sok Lee (UCSD: University of California, San Diego)H-Index: 27
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Summary The nature of obesity-associated islet inflammation and its impact on β cell abnormalities remains poorly defined. Here, we explore immune cell components of islet inflammation and define their roles in regulating β cell function and proliferation. Islet inflammation in obese mice is dominated by macrophages. We identify two islet-resident macrophage populations, characterized by their anatomical distributions, distinct phenotypes, and functional properties. Obesity induces the local exp...
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#1Marianne Böni-Schnetzler (University of Basel)H-Index: 18
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Summary Interleukin-1 receptor antagonist (IL-1Ra) is elevated in the circulation during obesity and type 2 diabetes (T2D) but is decreased in islets from patients with T2D. The protective role of local IL-1Ra was investigated in pancreatic islet β cell (βIL-1Ra)-specific versus myeloid-cell (myeloIL-1Ra)-specific IL-1Ra knockout (KO) mice. Deletion of IL-1Ra in β cells, but not in myeloid cells, resulted in diminished islet IL-1Ra expression. Myeloid cells were not the main source of circulatin...
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