Impaired CD4+ and T-helper 17 cell memory response to Streptococcus pneumoniae is associated with elevated glucose and percent glycated hemoglobin A1c in Mexican Americans with type 2 diabetes mellitus
ABSTRACT Individuals with type 2 diabetes are significantly more susceptible to pneumococcal infections than healthy individuals of the same age. Increased susceptibility is the result of impairments in both innate and adaptive immune systems. Given the central role of T-helper 17 (Th17) and T-regulatory (Treg) cells in pneumococcal infection and their altered phenotype in diabetes, this study was designed to analyze the Th17 and Treg cell responses to a whole heat-killed capsular type 2 strain of Streptococcus pneumoniae. Patients with diabetes demonstrated a lower frequency of total CD4+ T cells, which showed a significant inverse association with elevated fasting blood glucose. Measurement of specific subsets indicated that those with diabetes had, low intracellular levels of interleukin (IL)-17, and lower pathogen-specific memory CD4+ and IL-17+ cell numbers. No significant difference was observed in the frequency of CD4+ and Th17 cells between those with and without diabetes. However, stratification of data by obesity indicated a significant increase in frequency of CD4+ and Th17 cells in obese individuals with diabetes compared with nonobese individual with diabetes. The memory CD4+ T-cell response was associated inversely with both fasting blood glucose and percent glycated hemoglobin A1c. This study demonstrated that those with type 2 diabetes have a diminished pathogen-specific memory CD4+ and Th17 response, and low percentages of CD4+ T cells in response to S. pneumoniae stimulation.
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ABSTRACT: Alzheimer’s disease (AD), the most common form of dementia, is characterized by senile plaques, neurofibrillary tangles (NFT), and neuronal loss. Although many studies have focused on amyloid beta peptide (Ab) as a main toxin of AD, the exact mechanism of AD pathogenesisis not yet known. In this review, we focus on advanced glycation endproducts (AGEs) and their receptor (Receptor for AGEs [RAGE]) in AD pathogenesis. Several convincing pieces of evidence suggest that the blockade of AGEs and RAGE interactions is a promising therapeutic target for AD treatment.Edited by Reiko Inagi, 03/2014; International Maillard Reaction Society.