Abstract
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease
characterized by hyperglycemia. T2DM is caused by various etiologies.
The functional expansion of pancreatic β-cells is unable to compensate
for the degree of insulin resistance (IR), resulting in a relative
insulin deficiency. The onset and progression of T2DM are influenced by
multiple variables, including genetics, lipid excess, oxidative stress,
and inflammation. A growing body of research suggests that the
components of the immune system are altered in T2DM. This suggests that
T cell-mediated adaptive immunity stimulates inflammation and IR through
the redistribution of cytokines, chemokines, and different T cell
subsets. Metabolic inflammation is a central aspect of obesity, T2DM,
and comorbidities. This review focuses on adaptive immune T cells,
particularly CD4+ T cells, and examines the roles and effects of
different helper T (Th) 1, Th2, Th17, Th22, and regulatory T cells
(Tregs) in T2DM. Evidence for T cell activation and exhaustion in T2DM
remains controversial and requires further investigation.