A single chemical modality will have difficulty curing multidrug-resistant TB, eliminating holdover or dormant bacteria, and blocking TB resurgence. For this reason, the WHO strategic planning for tuberculosis research and development in the 1990s reintroduced a research program combining chemotherapy with immunization methods and recommended the use of Mycobacterium avium vaccine. Since the pathogenesis of tuberculosis and the understanding of protective immune mechanisms is still a challenge, there has been no breakthrough in research on immunization and treatment of tuberculosis, and the mechanisms of immunotherapy have, so far, not been clearly elucidated. Immunotherapy is still an empirical exploration. It is reported that more than 50% of TB patients have a combined damaged immune system, so immunotherapy is back to an important position. The goals of immunotherapy are 1. to improve the patient’s immune function (mainly T-lymphocytes and their cytokine assays). 2. to enhance the efficacy of chemotherapy, and 2. 2. Enhance the efficacy of chemotherapy, accelerate the conversion of sputum bacteria, and accelerate the absorption of lesions. 3. Shorten the course of chemotherapy and reduce side effects and complications. 4. Eliminate drug-resistant bacteria and dormant bacteria to prevent the recurrence of tuberculosis. Immunity mechanism of tuberculosis 1. Cellular immunity of tuberculosis When the antigen of tuberculosis bacteria, Mycobacterium tuberculosis or inoculated BCG first invades the body, it is firstly phagocytosed by macrophages, and the macrophages after phagocytosis of bacteria play three functions. (1) To kill Mycobacterium tuberculosis by releasing a variety of hydrolytic enzymes in vivo. (2) Produce and secrete various cytokines, mainly including IL-1, IL-6, IL-10, IL-15, TNF-α, TNF-β. (3) Uptake, process and present effective antigens to T lymphocytes. Thereafter, following the process of cellular immunity, T cells are sensitized by receiving the effective antigen, and when the same antigen invades again, the sensitized T cells release various cytokines to differentiate TD and TC precursor cells into TD and TC, thus exerting a cellular immune effect to kill and remove the invading Mycobacterium tuberculosis from the body. At the same time, the immune response inflammation also causes different degrees of damage to the body tissues. 2, type IV metaplasia caused by tuberculosis infection The principle of tuberculin test is a typical cell-mediated delayed metaplasia, that is, type IV metaplasia. Generally divided into two parts: specific and non-specific reactions. The specific reaction is that the injected local tuberculin stimulates the proliferation and differentiation of T lymphocytes sensitized by Mycobacterium tuberculosis or BCG and releases a variety of reactive lymphokines, and the chemotactic neutrophils and macrophages accumulate in the injected area to cause a local cellular infiltration dominated by late metaplastic cells and macrophages. The non-specific response is the infiltrating cells and the lymphokines released by them, resulting in a non-specific immune response to inflammation at the injection site. The combination of the infiltrating cells and the inflammatory response leads to a local erythema and hardness of the injection site after 24 hours, with a peak response at 48 to 72 hours. Later, the reaction decreases due to clearance of tuberculin and the injection site returns to normal.