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The below mentioned article provides a study note on Tumour Immunity:- 1. Evidence of Immune Mechanism in Malignancy 2. Tumour Antigens 3. Tumour Associated Transplantation Antigens (TATAS) 4. Mechanism of Immune Response to Tumours 5. Immune Surveillance.
Contents:
- Evidence of Immune Mechanism in Malignancy
- Tumour Antigens
- Tumour Associated Transplantation Antigens (TATAS)
- Mechanism of Immune Response to Tumours
- Immune Surveillance
1. Evidence of Immune Mechanism in Malignancy:
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1. Patients with certain immuno-deficiency disorder (e.g. congenital immuno-deficiency states) and patients undergoing chronic immuno-suppressive therapy seem to be more prone to increased incidence of cancer—particularly of the mononuclear phagocyte (i.e. lymphomas).
2. Spontaneous regression metastases after surgical removal of the primary tumour or recovery that sometimes follow chemotherapy of choriocarcinoma and Burkitt’s lymphoma—they suggest the role of tumour immunity. Spontaneous regression of tumour has been observed with neuroblastoma and malignant melanoma.
3. The phenomenon of immunological enhancement in tumour transplants.
4. Evidence of anti-tumour reactions are found in certain cancers by the presence of lymphocytes, plasma cells and macrophages after infiltrating the stroma simulating the cellular response of allograft reactions.
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2. Tumour Antigens:
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Tumour specific antigens are present on the membrane of cancer cells. When syngeneic animal is injected with such tumour specific antigens which reject the human transplant in immunized hosts, it is referred to as Tumour Specific Transplantation Antigen (TSTA).
In human beings, few tumours are caused by viruses. It is now evident that, in most cases of tumours, there is genetic alterations such as mutation, gene amplification, chromosomal deletion or translocation. Some of these genetic alterations lead to expression of altered proteins in tumour cells which probably serve as antigenic targets for mounting immune responses by the host.
3. Tumour Associated Transplantation Antigens (TATAS):
There are two types of TATAS:
1. Shared Tumour Antigens:
These antigens are shared by many tumours. They are found on tumours induced by viruses e.g. small DNA of polyoma viruses, SY 40 viruses and the papilloma viruses.
2. Tumour Specific Transplantation Antigens (TSTA):
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These antigens specific to an individual tumour can provoke an immune response to injected tumour cells, but only if the animal has been previously immunized with the same tumour.
The following are considered as the immunological expression of tumours:
Virally induced antigens: virus induced tumour cells express three types of antigens:
(a) “V” antigen is associated with the virion.
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(b) Tumour (T) or nuclear antigen is located in the nucleus of infected tumour cells and are specific for inducing virus and not the tumour.
(c) TSTA antigen or cytoplasmic membrane antigens are important as these come in contact with immune system. All tumours induced by specific virus contain the same TSTA even when the tumours are in different animal species.
This is in contrast to the case with chemically induced tumours in which TSTA is private (tumour specific) to a particular neoplasm, i.e. different tumours produced by a single chemical possess different antigens.
(II) Embryonic Antigens:
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Certain tumours in adults contain antigen found in foetal or embryonic cells but not corresponding normal adult cells, e.g. Carcino Embryonic Antigen (CEA) detected in serum of patients with neoplasm of gut (colonic cancers) and alpha fetoproteins present in serum of patients with hepatoma and testicular embryonic carcinoma.
The carcinoembryonic antigen (CEA) is a glycoprotein. In some malignancies, a metabolic shift of the cancerous cell from an adult to immature pathway of protein synthesis occurs leading to rise of embryonic Ag in serum.
As CEA also appears in serum of patients with alcoholic cirrhosis, its detection has limited diagnostic value. Alpha fetoprotein (alpha globulin) is produced by normal foetal (embryonic) hepatocytes and its serum level sharply declines after birth and is virtually absent in normal adult blood. It appears in blood in high concentration in hepatic carcinoma.
(III) Idiotypic Antigen:
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As already mentioned, tumours induced by chemical agents (e.g. benzopyrene) possess tumour specific (provate) own idiotypic antigen. For example, two anatomically distinct tumours induced on a single animal (mouse) by one chemical carcinoma will contain two antigenically distinct TSTA.
4. Mechanism of Immune Response to Tumours:
Resistance to tumour growth is offered primarily by cell mediated immunity. Specific tumour resistance can be passively transferred to normal animal using lymphoid cells from immunized animals. The sensitized T-cells attack the foreign tumour cells and tend to limit their growth. The transferred natural killer cells can also kill some of the tumour cells in absence of antibody.
The tumour antigens also induce humoral antibody production and some of these antibodies may be cytotoxic while others may facilitate the tumour growth by interfering with recognition and disposal of tumour cells by cell-mediated immunity of the host. Such interfering antibodies may produce an enhancement of tumour growth.
5. Immune Surveillance:
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It is held that malignant cells arise by mutation of somatic cells that occur frequently in the body. The concept of immune surveillance—first proposed by Ehrlich (1909) and by Burnet (1970)—stated that the immune system keeps a constant vigilance on each type of malignant mutation of somatic cells of individuals and destroy them on the spot.
Accordingly, the development of tumours represent an escape from this surveillance. This is perhaps an over-implication of a complicated issue. If this view was fully true there would have been higher incidence of tumours on patients receiving immuno-suppressive therapy.
