Impact of DM on TB prevention, diagnosis, and treatment from an immunologic perspective [TB0093]
One in every ten adults is a diabetic (DM) patient. Long-term hyperglycemia in DM patients leads to decreased immune cell numbers and function, increasing the incidence of tuberculosis (TB). Chronic hyperglycemia severely impairs the function of innate immune cells, affecting processes such as monocyte differentiation into macrophages and dendritic cells. This impairs the recruitment, recognition, phagocytosis, and antigen presentation functions of macrophages and reduces the frequency of dendritic cells and natural killer cells. Additionally, hyperglycemia increases the inflammatory response of neutrophils, which exacerbates bacterial load. Chronic hyperglycemia may delay the activation of adaptive immune cells, including CD4+ and CD8+ T cells. CD4+ T cells are crucial in anti-tuberculosis immunity, promoting the proliferation of T lymphocytes and macrophage activation via interferon-gamma (IFN-γ) secretion. However, high blood glucose levels can delay CD4+ T cell activation, reducing