Abstract
Diabetic nephropathy (DN) is one of the most significant microvascular complications in diabetic patients. DN is the leading cause of end-stage renal disease, accounting for approximately 50% of incident cases. The current treatment options, such as optimal control of hyperglycemia and elevated blood pressure, are insufficient to prevent its progression. DN has been considered as a nonimmune, metabolic, or hemodynamic glomerular disease initiated by hyperglycemia. However, recent studies suggest that DN is an inflammatory disease, and immune cells related with innate and adaptive immunity, such as macrophage and T cells, might be involved in its development and progression. Although it has been revealed that kidney dendritic cells (DCs) accumulation in the renal tissue of human and animal models of DN require activated T cells in the kidney disease, little is known about the function of DCs in DN. In this review, we describe kidney DCs and their subsets, and the role in the pathogenesis of DN. We also suggest how to improve the kidney outcomes by modulating kidney DCs optimally in the patients with DN.
Highlights
Diabetic nephropathy (DN) refers to microvascular complications and end-stage renal disease in diabetic patients, accounting for approximately 50% of incident cases [1]
Growing evidence suggest that inflammatory elements and infiltrating immune cells in both the innate and adaptive immune systems play a significant role in the pathogenesis of DN [4,5,6,7,8,9,10,11]
This study indicated that CD11c+ CD103+ DC subsets (cDC1s), but not cDC2s or plasmacytoid DCs (pDCs) play a pathogenic role via the activation of CD8+ T cells in adriamycin nephropathy (AN) [36,49]
Summary
Diabetic nephropathy (DN) refers to microvascular complications and end-stage renal disease in diabetic patients, accounting for approximately 50% of incident cases [1]. Murine cDC1s express several cell surface markers, the XCR1, CD103, and C-type lectin domain family 9 member A (CLEC9A; CD370) in nonlymphoid tissues and high levels of CD8 instead of the CD103 in lymphoid organs [19,22] They are described to cross-present exogenous antigens on MHC class I molecules to CD8+ cytotoxic T cells (CTLs). Mouse pDCs express high levels of plasmacytoid dendritic cell antigen-1 (PDCA-1), and human pDCs express the markers CD123 (interleukin-3 receptor), CD303 (BDCA2), and CD304 (BDCA4) Their unique function is sensing foreign or altered nucleic acids and the production of type 1 interferons during viral infections [29,30]. Monocytederived DCs are absent at the steady state and mainly arise in various inflammatory conditions [19,20]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
