Figure 1.

Schematic diagram of TB infection and anti-TB immunity of the host. APCs, such as DCs, macrophages, neutrophils, and even B cells, not only play the role of innate immune cells but also serve as a bridge between innate and adaptive immunity. DCs are the most important APCs, and their antigen presenting ability in vitro is 10-100 times that of other APCs. M. tuberculosis bacilli invading host’s pulmonary alveoli are first recognized and swallowed by APCs. Then, immature dendritic cells (iDCs) take up M. tuberculosis antigens and migrate to lymph nodes. During this process, the expression of MHC molecules on the surface is up-regulated, the antigen presentation function and the ability to activate T cells are also enhanced, and iDCs are transformed into mature dendritic cells (mDCs). mDCs can secrete interleukin-12 (IL-12), tumor necrosis factor-α (TNF-α), and interferon-α (IFN-α) to act on native CD4⁺ T cells (Th0 cells) to differentiate into Th1 cells. IFN-γ, IL-2, and TNF-α produced by Th1 cells can effectively activate CD8⁺ T cells and macrophages to eliminate intracellular M. tuberculosis by perforin, granzyme, reactive oxygen, and reactive nitrogen. Furthermore, mDCs produce IL-4, making Th0 cells differentiate into Th2 cells. The function of the Th2 response and lL-4 in the anti-tuberculosis immune response remains unclear. It is generally believed that Th2 cells will affect B lymphocytes by secreting IL-4, IL-5, and IL-10, mediating humoral immune response.