Basic Types of Immune Response
The body's defense against foreign agents is based on the coordinated work of two main systems. The character and intensity of any immune reaction directly depend on where the pathogen is localized and what its nature is.
- Innate immunity. This is a phylogenetically older system that provides the earliest stages of defense. It triggers instantly and represents a sort of "first line" of defense for the body against invasion.
- Adaptive (acquired) immunity. This type is activated somewhat later, but it is precisely this that plays a key role in increasing the overall efficiency of immune processes. In its effector phase, adaptive immunity demonstrates strict specificity to a specific pathogen. The most important result of its work is the formation of immunological memory, which allows the body to respond faster and more powerfully upon repeated encounter with the same pathogen.
Antitumor Surveillance and the Tolerance Phenomenon
The immune system not only fights infections but also monitors its own cells. Antitumor immunity is able to successfully recognize and eliminate many malignant cells at early stages. However, it exhibits weakness and cannot destroy an already fully formed tumor. The main reason for this lies in the absence of PAMP (pathogen-associated molecular pattern) expression on the surface of tumor cells. Notably, the absence of PAMP does not prevent the immune system from rejecting genetically foreign transplanted tissues.
In addition, there are special mechanisms in the body for restraining immune reactions—tolerance:
- Fetal tolerance. The fetus is genetically semi-allogeneic to the mother, yet its rejection does not occur. This is prevented by evolutionarily formed mechanisms that are inextricably linked with the functioning of the placenta.
- Immunologically privileged sites. These are special anatomical zones in the mammalian body that are isolated to varying degrees from the cells and factors of the immune system, preventing the development of inflammatory reactions there.
Autotolerance and Pathological Hyperactivity
Autotolerance is a crucial mechanism ensuring the protection of the body's own tissues from the damaging action of its own immune factors. The formation of this state occurs at several levels:
- Elimination of potentially dangerous autospecific lymphocyte clones in the thymus.
- Induction of anergy (unresponsiveness) in such cells in the periphery.
- Re-recombination of autospecific receptors so they stop recognizing "self".
- Blocking remaining active autospecific clones using specialized regulatory T lymphocytes.
If these delicate mechanisms of autotolerance are damaged, autoimmune processes develop, which underlie many severe diseases.
Another variant of pathology is allergy, a type of hypersensitivity representing a manifestation of increased, excessive activity of the immune system. The mechanism of allergy development is triggered when a specific antigen (allergen) interacts with IgE class antibodies that are pre-fixed on the surface of mast cells. This leads to an inadequate reaction: a massive release of mast cell granule contents and active synthesis of substances provoking allergy symptoms occur.
Immunodeficiencies and Malignancies
Impaired function of the immune system leads to the development of immunodeficiencies, which are divided into two large groups depending on the cause of occurrence.
Primary immunodeficiencies are always caused by genetic defects. Various gene mutations disrupt the normal development and adequate functioning of immune system cells from birth.
Acquired (secondary) immunodeficiencies develop during lifetime under the influence of various external and internal factors. The main causes of their formation include:
- Cytotoxic exposures.
- Prolonged starvation.
- Various metabolic disorders and severe endocrine pathologies.
- Infectious diseases, especially of viral etiology.
The most severe and well-known form of acquired immunodeficiency is HIV infection/AIDS. In this pathology, the virus directly infects and damages the immune system cells themselves, depriving the body of protection.
Furthermore, immune cells themselves can become a source of oncology. Leukemias and lymphomas are severe diseases that arise as a result of the malignant transformation of one's own immunocytes.
Briefly: answers to topical questions
Which target cells does the human immunodeficiency virus affect in HIV infection?
The human immunodeficiency virus affects cells that have the CD4 molecule on their surface, as well as a number of other cells. The main and additional target cells include:
- T-helper/amplifier cells (CD4+ T cells) are targets of the virus.
- Monocytes and macrophages do not die upon infection, but become a habitat and reproduction site for the pathogen.
- Dendritic cells belong to additional targets and tissue reservoirs of the virus.
- B lymphocytes: some of them are additional targets.
- Progenitor cells in the thymus and bone marrow are infected with HIV, which reduces regeneration.
- Neuroglial cells are primarily infected in the central nervous system; as a result, functional disorders, trophic damage to neurons and brain tissue develop.
What types of lymphocytes participate in blocking autospecific clones?
Natural regulatory T lymphocytes participate in blocking active autospecific clones. They provide dominant tolerance by suppressing reactive clones in the periphery. The main characteristics of these cells:
- Regulatory T lymphocytes (Treg) prevent the activation of autospecific effector T lymphocytes that escaped deletion and anergy.
- Membrane markers (CD4+, CD25hi, CTLA-4+) are specific molecules on the surface of these cells.
- Intracellular factor (FOXP3) is a key differentiation factor.
These lymphocytes escape negative selection in the thymus because their affinity threshold for autoantigen to trigger apoptosis is higher than that of other T cells. As a result, they do not die, but differentiate and emigrate to lymph nodes.
Levels of autotolerance formation: TAPR — Thymus (clone deletion), Anergy (in periphery), Recombination (of receptors), Regulatory T lymphocytes (blocking).
Class and exam questions
What is the main difference between innate and adaptive immunity?
Innate immunity works as the first line of defense at early stages, while adaptive is responsible for high reaction specificity in the effector phase and forms immunological memory.
Why doesn't the immune system destroy an established tumor?
The main reason for the weakness of the antitumor response at late stages is the absence of PAMP (pathogen-associated molecular pattern) expression on the surface of tumor cells.
How does an allergen trigger a hypersensitivity reaction?
The allergen interacts with IgE antibodies fixed on mast cells. This causes an inadequate reaction with the release of mast cell granule contents and the synthesis of active substances.
What factors cause secondary immunodeficiencies?
These include infections (especially viral ones, e.g., HIV), cytotoxic exposures, starvation, as well as endocrine pathologies and metabolic disorders.
What else to study on this topic
- The nature of pathogen-associated molecular patterns (PAMPs)
- Mechanisms of immunological memory formation
- Placental functioning in ensuring fetal tolerance
- Biochemistry of mast cell degranulation in allergy
- Genetic mutations underlying primary immunodeficiencies
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