Adaptive Immunity, Inflammation, and Cardiovascular Complications in Type 1 and Type 2 Diabetes Mellitus

Abstract

Diabetes mellitus (DM) is a pandemics that affects more than 170 million people worldwide, associated with increased mortality and morbidity due to coronary artery disease (CAD). In type 1 (T1) DM, the main pathogenic mechanism seems to be the destruction of pancreatic β-cells mediated by autoreactive T-cells resulting in chronic insulitis, while in type 2 (T2) DM primary insulin resistance, rather than defective insulin production due to β-cell destruction, seems to be the triggering alteration. In our study, we investigated the role of systemic inflammation and T-cell subsets in T1- and T2DM and the possible mechanisms underlying the increased cardiovascular risk associated with these diseases.

Predicting the Outcomes of Subjects With Severe Community-Acquired Pneumonia Using Monocyte Human Leukocyte Antigen-DR

“…[28][29][30][31] Only the number of malnourished subjects displayed a significant difference between the survivors and non-survivors. However, considering the limited number of malnourished subjects and limited association with mortality as shown by logistic regression, it could be deduced that severe community-acquired pneumonia was the main factor that caused the changes of mHLA-DR and mortality.…”

Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model

“…Diabetes mellitus is a chronic disease threatening the health of individuals worldwide (1). There are multiple, often serious, complications associated with diabetes mellitus, one of which is impaired healing, which can lead to a reduction in physical activity and, in certain cases, chronic wounds and limb amputation (1,2).…”

“…There are multiple, often serious, complications associated with diabetes mellitus, one of which is impaired healing, which can lead to a reduction in physical activity and, in certain cases, chronic wounds and limb amputation (1,2). An imbalance between the pro-and anti-inflammatory mediators accentuates diabetic vascular complications and impedes proper wound healing (3).…”

“…An imbalance between the pro-and anti-inflammatory mediators accentuates diabetic vascular complications and impedes proper wound healing (3). Other factors that contribute to deficient healing in patients with diabetes include altered host responses; attenuated antibacterial defenses; prolonged inflammation; changes in protease activity; insufficient cell production for rapid and robust healing; angiogenic disorders; decreased production of growth factors; inadequate extracellular matrix production; and changes in apoptosis (1)(2)(3)(4)(5).…”

“…The process is dependent upon a series of interactions between a variety of cell types, cytokine mediators and the extracellular matrix (1). In order for wound healing to be successful, a sufficient number of cells must be generated to participate in the repair (2,6,7).…”