Classification of defense mechanisms
In pathological physiology, three main groups of barriers are distinguished that prevent the development of neoplasms. Each of them is activated at a specific stage of the organism's interaction with the pathogen:
- Anticarcinogenic mechanisms are the first line of defense. Their main task is to prevent the interaction of the carcinogen with the genetic apparatus. This is achieved by creating obstacles to the penetration of carcinogens into the body, inside the cell, and directly into the nucleus, as well as by preventing their action on the genome.
- Antimutational mechanisms are the second line. They are aimed at protecting the genome and DNA repair if the carcinogen has nevertheless reached its target. They include detection, elimination of the oncogene, and suppression of its expression.
- Anticellular mechanisms are the third line. They are aimed at the elimination (removal) of already transformed cells. They ensure the detection of the tumor cell, inhibition of its growth, and final elimination.
Anticarcinogenic defense: chemical factors
This group of mechanisms performs three main functions: inhibition or blockade of the penetration of carcinogens into the cell and nucleus, prevention of their action on the genome, and inactivation and elimination of carcinogenic agents. Defense against chemical carcinogens is implemented in the following ways:
- Phagocytosis: active uptake and subsequent destruction of chemical carcinogens by phagocytic cells.
- Immunological inactivation: chemical blastomogenic agents act as haptens. Their inactivation occurs with the help of antibodies and T-lymphocytes, which ultimately leads to the destruction and elimination of the agents from the body.
- Competitive receptor blockade: non-carcinogenic metabolites bind to cellular receptors. This physically prevents the interaction of true carcinogens with the cell.
- Metabolic inactivation: destruction of carcinogens inside cells and in biological fluids. Includes processes of oxidation, reduction, and demethylation. An important role is played by physicochemical inactivation, in particular glucuronidation and sulfation.
- Removal from the body: inactivated substances are excreted with urine, feces, saliva, bile, and sweat.
Defense against viruses and radiation
The body possesses specific barriers against biological (viruses) and physical (radiation) factors.
Defense against oncogenic viruses prevents their penetration and replication:
- Humoral response: under the influence of viral antigens, plasma cells produce antibodies (Ig). They interact with the virus, blocking its contact with membrane receptors. The main effect is the prevention of transfection (penetration of viral nucleic acid into the nucleus) and subsequent tumor transformation.
- Action of interferons (IFN): these specific proteins inhibit or completely block the intracellular replication of viruses.
- Nonspecific cellular cytolysis: detection and destruction of virus-containing cells. Carried out by NK cells, cytotoxic T-lymphocytes, mononuclear phagocytes, dendritic cells, and astrocytes.
Antioxidant defense is aimed at neutralizing the products of radiolysis and free radical oxidation:
- Scavenging of free radicals (oxygen, lipids). The enzyme superoxide dismutase (SOD) catalyzes the reaction of oxygen radicals with hydrogen ions, forming hydrogen peroxide. Non-enzymatic "scavengers" also act: tocopherols and glutathione compounds.
- Destruction of peroxides and hydroperoxides (organic and inorganic compounds, lipids, proteins). This task is performed by endogenous anti-peroxide agents: catalases, glutathione peroxidases, and glutathione reductase.
Antimutational and anticellular mechanisms
It is important to remember: if anticarcinogenic mechanisms prove ineffective, oncogenes are activated, leading to tumor growth. In this case, internal reserves are activated:
- Antimutational mechanisms: their main goal is to ensure the detection, elimination, and/or suppression of oncogene activity. This defense is implemented through the participation of tumor suppressors (so-called "anti-oncogenes") and the active work of DNA repair enzyme systems.
- Anticellular mechanisms: if the cell has nevertheless mutated, the system proceeds to the elimination of transformed cells. The mechanisms are aimed at precise detection of the tumor cell, inhibition of its pathological growth, and complete elimination from the body.
Briefly: answers to topical questions
What specific anticellular mechanisms and tumor cell elimination factors exist?
Anticellular mechanisms of antitumor defense are aimed at detecting and eliminating transformed cells, as well as destroying genotypically/phenotypically foreign cells or inhibiting their growth.
They are classified into:
- Non-immune (nonspecific) — monitor the preservation of normal cell composition and are implemented by cells with cancerolytic properties and humoral factors.
- Immune (specific).
The elimination of tumor cells is carried out by factors of the immunobiological surveillance system. Defense factors include:
- killer cells;
- immunoglobulins (Ig);
- tumor necrosis factor alpha (TNF-α).
Interferons also have an antitumor effect: they activate NK cells, enhance MHC-I expression and tumor antigen presentation to T cells, suppress tumor cell proliferation, induce cell differentiation, and exert an antiangiogenic effect.
Which genes are classified as classical tumor suppressors (anti-oncogenes)?
Classical tumor suppressor genes (anti-oncogenes) include the Rb and p53 genes.
Their main function is to inhibit cell proliferation and initiate apoptosis. The Rb protein controls cell proliferation, and its loss leads to the development of retinoblastoma. The p53 protein is a phosphoprotein whose synthesis increases upon DNA damage, after which it halts the cell cycle for repair.
What are the molecular mechanisms of viral replication blockade by interferons?
Interferons block viral replication through intracellular cascades, inducing the synthesis of effector proteins:
- Induction of 2'5'-oligoadenylate synthetase — leads to the synthesis of 2'5'-oligoadenylates, activation of endoribonuclease (RNase L), and degradation of viral RNA.
- Induction of protein kinase R (P1 kinase) — activated by viral double-stranded RNA, phosphorylates cellular translation enzymes (factor eIF2$\alpha$), inhibiting transcription and translation, which blocks viral protein synthesis.
- Induction of Mx protein — forms cellular resistance to infection.
The rule of three "A"s for antitumor defense: Anticarcinogenic (keep the enemy away from DNA), Antimutational (repair DNA damage), Anticellular (destroy the cell if DNA is broken).
Class and exam questions
What happens if anticancer mechanisms fail?
Oncogenes will be activated, ultimately leading to uncontrolled tumor growth if the following lines of defense fail.
What role do interferons play in antitumor defense?
Interferons are proteins that inhibit or completely block the intracellular replication of oncogenic viruses, preventing cell transformation.
How does the body neutralize free radicals when exposed to radiation?
Free radicals are scavenged by enzymes (e.g., superoxide dismutase) and non-enzymatic factors (tocopherols). The resulting peroxides are then destroyed by catalase and glutathione peroxidase.
What else to study on this topic
- The role of NK cells and cytotoxic T-lymphocytes in cellular cytolysis.
- DNA repair mechanisms upon damage by carcinogens.
- Functions and types of tumor suppressors (anti-oncogenes).
- Glucuronidation and sulfation processes in metabolic inactivation.
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