Asistente de Investigación En Salud n/a, United States
Abstract: Type 2 diabetes (T2D) is characterized by chronic inflammation and in turn dysregulation of the immune system. The complexity of this inflammation is based on the fact that specific alterations in immune cell populations and subpopulations and their surface markers are yet not completely understood. Understanding the immunological profiles of these patients is necessary for the development of strategies to reduce the immune response and decrease the inflammation of these diseases. Demonstrating the importance of investigating the potential of stem cells for immunomodulation and effectiveness in this type of pathologies. The aim of this study was to characterize the immunological profile of T2D patients and evaluate the potential immunomodulatory effects of mesenchymal stem cells in this pathology. Methodology included collection of peripheral blood from both non-diabetics and diabetics patients, followed by isolation of peripheral blood mononuclear cells and analysis through flow cytometry to evaluate different immune cell populations and their markers. Our results showed that among the immunological alterations found in type 2 diabetic patients compared to control patients, CD8+CD127+ T lymphocytes and NK cells expressing NKGD2 show significantly elevated levels in type 2 diabetic patients. On the contrary, CD4+ T lymphocytes indicate a reduced expression of CXCR7 and CD127, intracellularly there is a decrease of INF-y and TNF-a in type 2 diabetic patients. Furthermoret, subpopulation of monocytes in tT2D showed an increase in IFN-y production, while NK cells showed a reduced production of TNF-a. Gene expression analysis reveals that diabetic patients showed a lower basal state of inflammatory mediators (IL-6, IDO, COX2) compared to non-diabetics, without any significant decrease in the expression of CXCR7 and CD127. The present study demonstrates a significant imbalance in the immune profile of type 2 diabetic patients, characterized by an enhanced cytotoxic response and potentially compromised helper T-cell function, demonstrating that innate and adaptive immunity, together with the expression of modified inflammatory genes, could represent an avenue for developing new diagnostic and therapeutic strategies in type 2 diabetic patients.
Funding Source: National Secretariat of Science, Technology and Innovation (SENACYT), Panamanian Association for the Advancement of Science (APANAC), Gorgas Memorial Institute of Health Studies