THE RESPONSE OF THE ORGANISM TO THE TUMOR

THE RESPONSE OF THE ORGANISM TO THE TUMOR

THE RESPONSE OF THE ORGANISM TO THE TUMOR

 

 

The immune response to foreign antigens is represented by humoral (antibodies) and cellular mechanisms. Even the most intense humoral response is not able to prevent the growth of a tumor. At the same time, effector cells, such as T cells, macrophages and natural killers, have relatively effective antitumor potentials. The activity of effector cells is anti-gene-induced and rezunt-ing cells and cells and is supported by cytokines (interleukins, interferons). Despite the activity of effector cells, host immunoreactivity may not be sufficient to control the growth and spread of the tumor.

 

The T-cell is the main cell responsible for the direct recognition and elimination of tumor cells. T cells carry out immunological surveillance, proliferate and destroy the transformed tumor cells formed after recognition of tumor-associated antigens (TAA).The response of T cells to the tumor is modulated by other cells of the immune system; some require the presence of humoral antibodies directed against tumor cells (antibody-dependent cellular cytotoxicity) in order to initiate the interaction leading to the death of tumor cells. In contrast, T-suppressor cells inhibit the immune response directed against tumor cells.

 

Cytotoxic T-lymphocytes (CTL) recognize antigens on target cells and lyse these cells. These antigens can be proteins localized on the surface or intracellular proteins (for example, TAA) expressed on the surface in combination with class I molecules of the major histocompatibility complex (MHC). Tumor-specific CTLs have been found in neuroblastoma, malignant melanomas, sarcomas and colon, breast, cervical, endometrial, ovarian, testicular, kidney and nasopharyngeal carcinomas.

 

Natural killers (NK) are another population of effector cells that have antitumor activity. In contrast to CTL, NK do not have receptors for detecting antigens, but can recognize normal cells infected with viruses, or tumor cells.Their antitumor activity is called "natural", as it is not induced by specific antigens. The mechanism by which NK distinguish between normal and abnormal cells is being studied. There is evidence that MHC I class molecules on the surface of normal cells inhibit NK activity, which prevents cell lysis. Thus, by altering the expressed characteristics of MHC I class molecules, many tumor cells activate NK with subsequent lysis.

 

Macrophages can kill tumor cells when activated by a combination of factors including lymphokines (soluble factors) produced by T cells and interferon. They are less effective than the cytotoxic mechanisms of T cells. Under certain conditions, macrophages can present TAA to T-cells and stimulate a tumor-specific immune response.

 

Dendritic cells are antigen-presenting cells in barrier tissues (skin, lymph nodes). They play a central role in the initiation of a tumor-specific immune response. These cells perceive tumor-associated proteins, process them and present for T cells, which stimulates the response of CTL against the tumor. The presence of dendritic cells in tumor tissues correlates with a positive prognosis.

 

Lymphokines produced by immune cells stimulate growth or induce the activity of other immune cells. Such lymphokines are IL-2, also known as T-cell growth factor, and interferons. IL- is produced by dendritic cells and specifically induces CTL, which enhances the antitumor immune response.

 

Humoral immunity

 

 

In contrast to T-cell cytotoxic immunity, humoral antibodies do not provide significant protection against tumor growth. Most antibodies do not recognize TAA. Nevertheless, humoral antibodies that react with tumor cells in vitro are found in the serum of patients with various neoplastic processes, including Burkitt lymphoma, malignant melanoma, osteosarcoma, neuroblastoma, lung cancer, breast cancer and gastrointestinal tract.

 

Cytotoxic antibodies are directed against surface antigens of tumor cells. These antibodies are capable of activating antitumor effects by fixing complement or serve as a flag for the destruction of tumor cells by T-lymphocytes (antibodies-dependent cell-mediated cytotoxicity).Another population of humoral antibodies, called an amplifying antibody (blocking antibodies), is capable of supporting more than inhibiting tumor growth. The mechanisms and significance of such an immunological enhancement are not clear.

 

Host protection failure

 

 

Although many tumors are eliminated by the immune system (and thus never defined), others continue to grow, despite the presence of TAA. To explain this deficiency in the response of the host organism to TAA, several mechanisms have been proposed:

 

- specific immunological tolerance to TAA in a process involving antigen-presenting cells and T-cell suppressors, possibly secondary to the prenatal exposure of the antigen;

 

- suppression of the immune response by chemical, physical or viral agents (for example, T-helper cells are destroyed by HIV);

 

- suppression of the immune response by cytotoxic drugs or radiation;

 

- suppression of the immune response (reduction of T-, B- and antigen-presenting cell function, decrease in IL-2 production, increase in circulating soluble IL-2 receptors) directly by the tumor through various complex and largely unclear mechanisms.


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