Pathology of Diabetes-Induced Immune Dysfunction.
Michael AlexanderEric ChoEiger GliozheniYusuf SalemJoshua CheungHirohito IchiiPublished in: International journal of molecular sciences (2024)
Diabetes is associated with numerous comorbidities, one of which is increased vulnerability to infections. This review will focus on how diabetes mellitus (DM) affects the immune system and its various components, leading to the impaired proliferation of immune cells and the induction of senescence. We will explore how the pathology of diabetes-induced immune dysfunction may have similarities to the pathways of "inflammaging", a persistent low-grade inflammation common in the elderly. Inflammaging may increase the likelihood of conditions such as rheumatoid arthritis (RA) and periodontitis at a younger age. Diabetes affects bone marrow composition and cellular senescence, and in combination with advanced age also affects lymphopoiesis by increasing myeloid differentiation and reducing lymphoid differentiation. Consequently, this leads to a reduced immune system response in both the innate and adaptive phases, resulting in higher infection rates, reduced vaccine response, and increased immune cells' senescence in diabetics. We will also explore how some diabetes drugs induce immune senescence despite their benefits on glycemic control.
Keyphrases
- glycemic control
- type diabetes
- blood glucose
- low grade
- rheumatoid arthritis
- bone marrow
- cardiovascular disease
- endothelial cells
- weight loss
- dna damage
- oxidative stress
- insulin resistance
- immune response
- high glucose
- stress induced
- diabetic rats
- high grade
- mesenchymal stem cells
- drug induced
- metabolic syndrome
- disease activity
- ankylosing spondylitis
- adipose tissue
- skeletal muscle