IDENTIFICATION OF MICA/B EXPRESSION IN SERA OF TYPE 2 DIABETIC PATIENTS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The immune system may play an important role in the development of the pathological complications. It has been suggested that hyperglycemia in diabetes may cause various cell stresses and induce vessels to express activating ligands for immune cells and other inflammatory factors, which in turn recruit and activate immune cells, resulting in various pathological complications. We hypothesize that a couple of stress-induced proteins, MHC class I chain-related gene A and B (MICA/B), might be induced to express in the blood vessels and other tissues involved in the activation of immune cells in diabetic patients. MICA/B may stimulate or co-stimulate various immune cells, such as natural killer cells and gamma/delta T cells, through interaction with their receptor, NKG2D. We have found that upregulation of ligands for NKG2D in blood vessels of diabetic mice and would like to study whether MICA and B are upregulated in human diabetic patients. Since it has been reported that MICA/B could shed into the circulatory system when expressed, we will collect blood samples from diabetic patients and measure amounts of MICA/B proteins in these blood samples by enzyme-linked immunosorbent assay (ELISA) with specific antibodies against MICA/B. This study may help us to understand molecular mechanisms of development of the various pathological complications in diabetic patients and could provide biomarkers for progression of these diabetes-related complications.