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HUMORAL IMMUNE RESPONSE IN TUBERCULOSIS INFECTION 
Nazarov J.S. 
Bukhara State Medical Institute, Bukhara, Republic of Uzbekistan. 
[e-mail]
 
The history of coexistence of mycobacteria, causative agents of 
tuberculosis, and humanity has thousands of years, and all this time, 
tuberculosis takes an annual tribute in the form of hundreds of thousands of 
human lives. According to the World Health Organization, up to 10 million 
people fall ill with tuberculosis every year, and about 1.5 million people die 
from this disease. Against the background of this disease, many scientific 
studies have noted that 98% of patients with tuberculosis have an immune 
imbalance. The paradox of the immune response to M. tuberculosis is the 
simultaneous activation and anergy of immunocompetent cells. Humoral 
immunity of the human body is not of decisive importance, due to the fact that 
mycobacteria find "refuge" inside macrophages. Nevertheless, humoral 
immunity is manifested by the synthesis of antibodies to antigens of 
mycobacteria. Circulating immune complexes (CIC) are formed, with the help 
of which antigens are eliminated from the body. A non-sterile form of immunity 
is formed, acting only when there is a pathogen in the body. Virulent 
mycobacteria have evolved the ability to desensitize macrophages to IFN-γ 

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(macrophage activator). The formation of high protective immunity in 
tuberculosis is associated with the response of Th1, which produce IFN-γ, and 
low resistance to infection is associated with the activity of Th2, which secrete 
IL-4. It is interleukin 4 that is responsible for the decrease in the production of 
Th1 cells, macrophages, IFN-γ, and dendritic cells. Hyperproduction of IL-4 is 
directly related to airway inflammation and allergies. IL-4 induces a class 
switch of B cells to increase IgE production. It was revealed that the increased 
content of total serum IgE in tuberculosis correlates with the severity of the 
disease and the effectiveness of therapy. 
Strengthening of the humoral link of immunity, against the background of 
moderate inhibition of the T-system, indicates the progression of the 
tuberculous process or its chronicity. Often, the progression of tuberculosis 
infection occurs with an uncontrollably high production of anti-inflammatory 
cytokines. The presence in the blood of tuberculosis patients of an increased 
number of T-lymphocytes containing intracellular IFN-γ, compared with 
healthy donors and carriers of latent infection, indicates a mycobacterial load 
and can be used to diagnose tuberculosis. IFN-γ stimulates macrophages and 
potentiates the death of intramacrophage bacteria, restoration of the level of 
IFN-γ induction in patients with tuberculosis during treatment leads to positive 
clinical dynamics. Thus, studying the mechanisms of humoral immunity in 
tuberculosis can help decide to what extent the activation or death of different 
populations of immune cells serves as a protective or pathological process in the 
human body. In addition, the clarification of the mechanisms will undoubtedly 
increase the level of diagnosis of tuberculosis infection.