Abstract
Enhanced expression of chemotactic cytokines (aka chemokines) within pancreatic islets likely contributes to islet inflammation by regulating the recruitment and activation of various leukocyte populations, including macrophages, neutrophils, and T-lymphocytes. Because of the powerful actions of these chemokines, precise transcriptional control is required. In this review, we highlight what is known about the signals and mechanisms that govern the transcription of genes encoding specific chemokine proteins in pancreatic islet β-cells, which include contributions from the NF-κB and STAT1 pathways. We further discuss increased chemokine expression in pancreatic islets during autoimmune-mediated and obesity-related development of diabetes.
Highlights
The dysfunction and ultimate reduction of total numbers of pancreatic islet -cells is central to the development of both Type 1 (T1DM) and Type 2 diabetes mellitus (T2DM)
Pancreatic islets isolated from various rodent models of diabetes reveal the expression of genes linked to immune cell recruitment and -cell dysfunction; islets isolated from human diabetic subjects show similar elevated gene expression patterns (Table 1)
If this inflammation does not resolve, eventual losses in overall function and total numbers of islet -cells leads to overt hyperglycemia, sine qua non for diagnosis of diabetes mellitus
Summary
The dysfunction and ultimate reduction of total numbers of pancreatic islet -cells is central to the development of both Type 1 (T1DM) and Type 2 diabetes mellitus (T2DM). T1DM is typically associated with autoimmune-mediated mechanisms that selectively eliminate the insulin-positive -cells within the pancreatic islets [1]. T2DM is correlated with obesity and is usually preceded by a period of insulin resistance and glucose intolerance prior to the loss in function islet -cell mass that leads to the development of overt diabetes [2,3]. Biomolecules 2015, 5 of T1DM is clearly different than that of T2DM, inflammation-associated damage and dysfunction of pancreatic islet -cells appear to be important components of each endocrine disease subtype. The rise in the number of publications over the last 15 years reveals the trends in research efforts related to these topics (Figure 1)
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