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.