Cellular Immunity of Patients with Tuberculosis Combined with Diabetes

Abstract

Tuberculosis (TB) is one of humanity's three major infectious diseases. Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia due to impaired insulin secretion or impaired insulin function. It has been reported that DM is a primary risk factor for TB disease. Given the increasing public health threat to people's health, more and more studies have focused on diabetes complicated by TB. Hyperglycemia can affect the function of human immune cells, promote primary infections and reactivation of TB, and increase the susceptibility and severity of TB. However, the immunological mechanism behind it is still not clear. By reviewing the related articles on tuberculosis complicated with diabetes published in recent years, this paper expounds on the effect of hyperglycemia on innate immunity and adaptive immunity of patients with TB. This review provides new insights for elucidating the immunological mechanism of TB complicated with DM and lays the foundation for finding potential targets for preventing and treating TB combined with DM.

Figure 1

Pathogenesis of T1DM and T2DM. In healthy people, insulin binds to insulin receptors and activates the opening of glucose transporter channels in fat/muscle cells, thereby reducing blood glucose levels. In T1DM, pancreatic cells are unable to produce insulin and therefore cannot bind to insulin receptors to induce glucose transporters to remove glucose from the blood. In people with T2DM, chronic overproduction of insulin leads to desensitization of insulin receptors so that glucose transporters cannot be activated to remove glucose from the blood.

Figure 2

Effects of hyperglycemia on host clearance and killing of M. tuberculosis. (a)Schematic diagram of M. tuberculosis infection. (b) Pathogenesis of T2DM. (c) Effect of hyperglycemia on the immunity of TB patients.