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.

Diabetes is a chronic disease that induces many comorbidities, including cardiovascular disease, nephropathy, and liver damage. Many mechanisms have been suggested as to how diabetes leads to these comorbidities, of which increased oxidative stress in diabetic patients has been strongly implicated. Limited knowledge of antioxidative antidiabetic drugs and substances that can address diabetic comorbidities through the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway calls for detailed investigation. This review will describe how diabetes increases oxidative stress, the general impact of that oxidative stress, and how oxidative stress primarily contributes to diabetic comorbidities. It will also address how treatments for diabetes, especially focusing on their effects on the Nrf2 antioxidative pathway, have been shown to similarly affect the Nrf2 pathway of the heart, kidney, and liver systems. This review demonstrates that the Nrf2 pathway is a common pathogenic component of diabetes and its associated comorbidities, potentially identifying this pathway as a target to guide future treatments.

This review will focus on how ethnic consumption of foods such as shiitake, ginseng, turmeric, black seeds, berries, rosemary, moringa and holy basil can help act as antioxidants and immune modulators in fighting many diseases. We will investigate how these foods act on pathways like Nrf2/Keap1 to increase endogenous antioxidant capacity and help in reducing ROS production, based on publications found in PubMed between 1994 and 2024. In addition, we will show how these plants can cause immune system shifts by changing the makeup of the ratio of Th1/Th2 cells, reduce inflammation, and have antiangiogenic effects on cancer. This review will also show how plants can alter the gut microbiota and lead to a further decrease in oxidative stress. Overall, it will show how plants and their metabolites can potentially create a path forward for creating novel therapeutic approaches and help lead to an improved redox balance, support immune function, and enhance long-term health outcomes.