Circulating dendritic cell number and intracellular TNF-a production in women with type 2 diabetes
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Sally E. Blank Emily Carolyn Johnson Debra K. Weeks Carol H. Wysham
- چاپ و سال / کشور: 2010
Description
Human dendritic cell (DC) subsets perform specialized functions for surveillance against bacterial and viral infections essential for the management of type 2 diabetes (T2D). Production of tumor necrosis factor-alpha (TNF-a) by DCs acts in autocrine fashion to regulate DC maturation and promotes the inflammatory response. This study was designed to compare circulating DC number and intracellular TNF-a production between post-menopausal women with T2D and healthy women. Blood samples were obtained (n = 21/group) and examined for plasma glucose and TNF-a concentrations, and dendritic cell subset immunophenotype (plasmacytoid, pDC, CD85k(ILT-3)? CD123?CD16-CD14- and myeloid, mDC, CD85k(ILT-3)? CD33?CD123dim to negCD16-CD14dim to neg). Intracellular production of TNF-a was determined in unstimulated and stimulated DCs. Women with T2D had significantly (P\0.05) greater plasma glucose and TNF-a concentrations when compared to healthy women. Women with T2D having poor glycemic control (T2D Poor Control, HbA1c C 7%) had fewer circulating pDCs than women with T2D having good glycemic control (T2D Good Control, HbA1c\7%) and healthy women. A significant interaction (P = 0.011) was observed between the effects of plasma glucose and group for intracellular expression of TNF-a in stimulated pDCs. Intracellular production of TNF-a in pDCs was significantly greater in healthy vs. T2D Poor Control (P\0.0001) and T2D Good Control (P\0.0001) but did not differ between T2D subgroups. The mDC number and intracellular production of TNF-a did not differ between groups. These findings indicate that TNF-a production by pDCs was reduced in women with T2D and circulating number of pDCs was associated with glycemic control.
Acta Diabetol DOI 10.1007/s00592-010-0190-8 Received: 19 October 2009 / Accepted: 29 March 2010 Springer-Verlag 2010
