Hyperglycemia Alters the CD27:CD70 Axis of Human Immune Cells

Abstract Introduction/Objective The exact mechanism that inflammation plays in the pathogenesis from obesity to Type 2 diabetes is unclear, however, activated immune cells and pro-inflammatory cytokines have been found adipose tissue of diabetics, implicating their role disease process. While CD27-CD70 axis being explored other models chronic inflammation, such as rheumatoid arthritis colitis, played remains unknown. Objective Evaluate whether hyperglycemia alters phenotype effector function, specifically CD27:CD70 on human cells. Methods/Case Report Human peripheral blood donors was divided into three groups. n=40 total those a healthy glucose value are without any co-morbidities (normoglycemic), patients identified having pre-diabetes per hemoglobin A1c (HgbA1c) (5.6-6.5%), with diabetes, an elevated HgbA1c (> 6.5%). then stained monoclonal antibodies towards cell surface markers associated including CD27/CD70 analyzed via flow cytometry. Previous data using cultures PBMC-derived T autologous dendritic exposed varing concentrations simulate compared this data. Results (if Case Study enter NA) 1) directly pre-diabetic individuals down-regulate CD27 expression. CD70 up-regulated individual when normoglycemic individuals. In accordance above resutls, CD4 after co-culture stimulated This includes down-regulation up-regulation Conclusion Our shows certain and/or diabetic patients. Specifically, we demonstrate novel evidence or hyperglycemic conditions. These molecules may offer potential target for therapeutics. Alternatively, our findings would allow further way characterize where patient spectrum between full-blown diabetes.