Methylglyoxal: possible link between hyperglycaemia and immune suppression?
No matter the cause of diabetes, the result is always hyperglycaemia. This excess glucose metabolism drives several damage pathways and raises concentrations of the reactive dicarbonyl, methylglyoxal (MG). MG can modify the structure and function of target molecules by forming advanced glycation end-products (AGEs) that act through their receptor (RAGE) to perpetuate vascular and neuronal injury responsible for long-term complications of diabetes. Diabetes patients also suffer lower resistance to many common infections, although the cause(s) for this lower resistance remains elusive. Here, we review recent evidence concerning immune suppression in diabetes and discuss the effects of MG on components of the immune system. We suggest that MG could be a missing link between hyperglycaemia and immune suppression in diabetes.
Price
Claire L
CL
Antigen Presentation Research Group, Imperial College London Faculty of Medicine, Level 7W, NWLH campus, Watford Road, Harrow, Middlesex, HA1 3UJ, UK.
Knight
Stella C
SC
D000818:Animals; D003920:Diabetes Mellitus / Q000276:immunology / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000276:immunology / Q000378:metabolism*; D007155:Immunologic Factors / Q000276:immunology / Q000378:metabolism*; D007165:Immunosuppression Therapy; D018384:Oxidative Stress / Q000502:physiology; D011765:Pyruvaldehyde / Q000276:immunology / Q000378:metabolism*
D017127:Glycation End Products, Advanced; D007155:Immunologic Factors; D011765:Pyruvaldehyde