PT  - JOURNAL ARTICLE
AU  - Iwai, Naomi
AU  - Steib, Catherine
AU  - Marzo, Amanda
AU  - Lerret, Nadine M.
TI  - The Role of Hyperglycemia in CD4 T-Cell Survival and Differentiation
AID  - 10.29074/ascls.2018000331
DP  - 2018 Apr 01
TA  - American Society for Clinical Laboratory Science
PG  - 52--58
VI  - 31
IP  - 2
4099  - http://hwmaint.clsjournal.ascls.org/content/31/2/52.short
4100  - http://hwmaint.clsjournal.ascls.org/content/31/2/52.full
SO  - Clin Lab Sci2018 Apr 01; 31
AB  - The major driving force in the pathogenesis of prediabetes and type 2 diabetes is thought to be chronic and low-grade systemic inflammation. Immune cells are key players in the induction of this chronic inflammation; however, the type of immune cells and mechanisms underlying the rapidly progressing pathogenesis of this disease are unclear. Therefore, we examined whether hyperglycemia alters CD4 T-cell activation, differentiation, and survival. Dendritic cells and T cells were isolated from human peripheral blood and cultured with varying amounts of glucose. Using flow cytometry, we found dendritic cells primed in hyperglycemic conditions induced CD4 T cells to exhibit a more activated phenotype capable of mobilization. This was evident by upregulation of the adhesion molecule CD11a. Additionally, these activated CD4 T cells had a lower degree of proliferation and decreased expression of the apoptotic protein caspase-3 compared with CD4 T cells primed by dendritic cells stimulated with a physiological concentration of glucose. We conclude that hyperglycemia drives CD4 T cells toward an activated immunophenotype, which could be assessed via flow cytometry in the clinic to further stratify patients with prediabetes and type 2 diabetes and potentially predict those patients at highest risk for progression of the disease.