Dog IgG (Fab'2) [HRP]

Advanced glycation endproducts (AGEs) are formed in a series of non-enzymatic reactions between reducing sugars and the amino groups of proteins and accumulate during aging, diabetes mellitus, chronic kidney disease and other chronic diseases. Accumulation of AGE-modifications alters protein structure and function, transforming these molecules into potential targets of the immune system, presumably triggering the production of autoantibodies against AGEs. In this study, we detected autoantibodies against AGE-modified proteins with ELISA in plasma samples of 91 patients with documented coronary artery disease (CAD), who underwent coronary artery bypass grafting (CABG) surgery. Patients with high levels of autoantibodies had a higher body mass index (BMI 28.6 vs 27.1 kg/m(2); p=0.046), were more likely to suffer from chronic obstructive pulmonary disease (COPD 30% vs 9.8%; p=0.018), and more likely to need dialysis after the surgery (10% vs 0%; p=0.037). Our findings show a weak link between the levels of autoantibodies against AGEs and diabetes mellitus (DM 44% vs 24.4%; p=0.05). In a small subpopulation of patients, antibodies against native bovine serum albumin (BSA) were detected. A growing body of research explores the potential role of antibodies against AGE-modified proteins in pathogenesis of different chronic diseases; our data confirms the presence of AGE-autoantibodies in patients with CAD and that in parallel to the AGEs themselves, they may have a potential role in concomitant clinical conditions in patients undergoing CABG surgery. Further research is necessary to verify the molecular role of these antibodies in different pathological conditions.

The characterization of cell-mediated and humoral adaptive immune responses to SARS-CoV-2 is fundamental to understand COVID-19 progression and the development of immunological memory to the virus. In this study, we detected T-cells reactive to SARS-CoV-2 proteins M, S, and N, as well as serum virus-specific IgM, IgA, IgG, in nearly all SARS-CoV-2 infected individuals, but not in healthy donors. Virus-reactive T cells exhibited signs of in vivo activation, as suggested by the surface expression of immune-checkpoint molecules PD1 and TIGIT. Of note, we detected antigen-specific adaptive immune response both in asymptomatic and symptomatic SARS-CoV-2 infected subjects. More importantly, symptomatic patients displayed a significantly higher magnitude of both cell-mediated and humoral adaptive immune response to the virus, as compared to asymptomatic individuals. These findings suggest that an uncontrolled adaptive immune response contribute to the development of the life-threatening inflammatory phase of the disease. Finally, this study might open the way to develop effective vaccination strategies.