Nonspecific resistance of the macroorganism is provided by the phagocytic activity of micro- and macrophages.
Phagocytosis (from the Greek phago - eat, cytos - cell) is the most ancient resistance mechanism that operates at all stages of the evolution of the animal world. In the simplest organisms, it simultaneously provides the functions of nutrition (absorption, digestion) and protection of cells. At the highest stages of evolution, phagocytosis thus performs only protective functions with the help of a differentiated system of cells. Phagocytosis is the process of active absorption by the cells of the body of pathogenic living or killed microbes and other foreign particles that enter it, followed by digestion with the help of intracellular enzymes.
Phagocytic cells fall into two main categories:
m and kr about ph and g, or polymorphonuclear phagocytes (PMN), and
m and kr about ph and, or mononuclear phagocytes (MN). The vast majority of phagocytic PMNs are neutrophils. Among macrophages, mobile (circulating) and immobile (sedentary) cells are distinguished. Motile macrophages are peripheral blood monocytes, while immobile macrophages are liver, spleen, and lymph node macrophages lining the walls of small vessels and other organs and tissues.
One of the main functional elements of micro- and macrophages are lysosomes - granules with a diameter of 0.25 ... 0.5 microns, containing a large set of enzymes (acid phosphatase, B-glucuronidase, myeloperoxidase, collagenase, lysozyme, etc.) and a number of other substances (cationic proteins, phagocytin, lactoferrin) capable of participating in the destruction of various antigens.
The process of phagocytosis includes the following stages: chemotaxis and adhesion (adhesion) of particles to the surface of phagocytes; gradual immersion (capture) of particles into the cell, followed by separation of a part of the cell membrane and the formation of a phagosome; fusion of phagosomes with lysosomes; enzymatic digestion of trapped particles and removal of remaining microbial elements.
The activity of phagocytosis is associated with the presence of opsonins in the blood serum. Opsonins are normal blood serum proteins that combine with microbes, making the latter more accessible to phagocytosis. There are thermostable and thermolabile opsonins. The former mainly relate to immunoglobulin G, although opsonins related to immunoglobulins A and M can also contribute to phagocytosis. Thermolabile opsonins (destroyed within 20 minutes at a temperature of 56 ° C) include components of the complement system - C1, C2, C3 and C4.
Phagocytosis, in which the death of a phagocytosed microbe occurs, is called complete (perfect). Phagocytosis, when in some cases the microbes inside the phagocytes do not die, is called incomplete.
The subsequent development of the phagocytic theory amended the ideas of I. I. Mechnikov about phagocytosis as a universal and dominant mechanism of protection against all existing infections.
Control questions and tasks. 1. What is immunology? 2. Define immunity. 3. Name the humoral factors of nonspecific protection. 4. What is a complement? Name the pathways of complement activation. What is their feature? 5. What is interferon? Name its main properties. 6. Tell us about the inhibitors found in the blood serum. 7. What is meant by the term "bactericidal activity of blood serum" (BAS), due to what components does it manifest itself? 8. What is phagocytosis? Name the phagocytic cells. 9. What is the difference between completed and incomplete phagocytosis?
Immunity is understood as a set of processes and mechanisms that provide the body with a constancy of the internal environment from all genetically alien elements of exogenous and endogenous nature. Nonspecific resistance factors are manifestations of innate immunity. Allocate: mechanical barriers(skin, mucous membranes), humoral factors(immunocytokines, lysozyme, beta-lysins, properdin protein system, acute phase proteins) and cellular factors(phagocytes, natural killers). Unlike immunity, nonspecific resistance is characterized by:
1) Lack of a specific response to certain antibodies;
2) The presence of both inducible and non-inducible protection factors;
3) Lack of ability to retain memory from initial contact with the antigen.
The main cell effector cells in the destruction of microbes are phagocytes (neutrophils, macrophages). However, the functions of phagocytes are not limited to the killing of a foreign particle. The phagocyte performs 3 main groups of functions:
1) Protective(proper phagocytosis)
2) Representing- macrophage presents AG to lymphocytes in the system of cellular cooperation
3) Secretory- produces more than 60 active mediators, including IL-1.8; reactive oxygen species, metabolic products of arachidonic acid, etc.
With the development of insufficient activity of any of the factors of nonspecific resistance, an immunodeficiency state develops, and therefore it is necessary to have an idea about the ways to assess the functional activity of each of the above components.
Scheme 1. Main methods for assessing the various stages of phagocytosis.
1. Take into account the results of crops of dissected animals. Calculate the total contamination in different sectors, fill in the table of contamination in different organs and tissues of the experimental animal in a notebook.
2. Describe the colony (at the choice of the teacher) according to the standard scheme (see the topic ‘Bacteriological research method’).
3. Prepare smears and stain them according to Gram. Mikoscopy, characterize the morphological picture.
4. To study the picture of incomplete phagocytosis in finished preparations.
5. Analyze the scheme for setting up the phagocytosis experiment.
6. Disassemble the scheme of staging the opson-phagocytic reaction.
Control questions:
1. List the main groups of nonspecific resistance factors.
2. Describe the anatomical barriers of nonspecific resistance.
3. What are the main differences between nonspecific resistance and immunity.
4. Describe humoral nonspecific resistance factors (lysozyme, immunocytokines, complement, beta-lysins, properdin system, acute phase proteins)
5. Complement system: structure, functions, types of activation?
6. What cellular factors of nonspecific resistance do you know?
7. Describe the stages of phagocytosis.
8. What are the forms of phagocytosis.
9. What are the mechanisms of phagocytosis.
10. Describe the main forms of free radicals.
11. What is phagocytic index and phagocytic number. Assessment methods.
12. What methods can additionally assess the activity of a phagocyte?
13. Method for assessing intracellular killing: clinical significance, setting.
14. Essence of opsonization. Phagocytic-opsonic index.
15. NST-test: setting, clinical significance.
16. Significance of anti-lysozyme, anti-complementary, anti-interferon activities of bacteria.
TOPIC 3. IMMUNE REACTIONS (1 LESSON)
One form of immunological reactivity is the body's ability to produce antibodies in response to an antigen. An antigen is a substance of a certain chemical structure that carries foreign genetic information. Antigens are complete, that is, able to cause the synthesis of antibodies and bind to them, and defective or haptens. Haptens can only bind to the antibody, but not cause its synthesis in the body. Bacteria and viruses are represented by a complex system of antigens (tables 4.5), some of them have toxic and immunosuppressive properties.
Table 4
Bacterial antigens
Table 5
Virus antigens
Immunological research methods- diagnostic research methods based on the specific interaction of antigens and antibodies. Widely used for laboratory diagnosis of infectious diseases, determination of blood groups, tissue and tumor antigens, protein species, recognition of allergies and autoimmune diseases, pregnancy, hormonal disorders, as well as in research work. They include serological reactions, which usually include reactions of direct exposure to antigens and antibodies in blood serum in vitro. Depending on the mechanism, serological reactions can be divided into reactions based on the phenomenon of agglutination; reactions based on the phenomenon of precipitation; lysis reactions and neutralization reactions.
Reactions based on the phenomenon of agglutination. Agglutination is the gluing of cells or individual particles - carriers of an antigen with the help of immune serum to this antigen. Bacterial agglutination reaction with the use of an appropriate antibacterial serum is one of the simplest serological reactions. A suspension of bacteria is added to various dilutions of the tested blood serum and after a certain contact time at t° 37° register at what highest dilution of blood serum agglutination occurs. There are fine-grained and coarse-grained agglutination reactions. When binding through the H-antigen of bacteria, a precipitate is formed from large ar-at conjugates, in the form of flakes. Upon contact with O-ar, a fine-grained precipitate appears. The agglutination reaction of bacteria is used to diagnose many infectious diseases: brucellosis, tularemia, typhoid fever and paratyphoid fever, intestinal infections, and typhus.
The reaction of passive, or indirect, hemagglutination(RPGA, RNGA). It uses erythrocytes or neutral synthetic materials (for example, latex particles), on the surface of which antigens (bacterial, viral, tissue) or antibodies are adsorbed. Their agglutination occurs when the appropriate sera or antigens are added. RBCs sensitized with antigens are called antigenic erythrocyte diagnosticum and are used to detect and titrate antibodies. Erythrocytes sensitized by antibodies. are called immunoglobulin erythrocyte diagnosticums and are used to detect antigens. The passive hemagglutination reaction is used to diagnose diseases caused by bacteria (typhoid and paratyphoid, dysentery, brucellosis, plague, cholera, etc.), protozoa (malaria) and viruses (influenza, adenovirus infections, viral hepatitis B, measles, tick-borne encephalitis, Crimean hemorrhagic fever, etc.).
Reactions based on the phenomenon of precipitation. Precipitation occurs as a result of the interaction of antibodies with soluble antigens. The simplest example of a precipitation reaction is the formation of an opaque precipitation band in a test tube at the border of antigen layering on an antibody. Various types of precipitation reactions in semi-liquid agar or agarose gels are widely used (Ouchterlony double immunodiffusion method, radial immunodiffusion method, immunoelectrophoresis), which are both qualitative and quantitative. As a result of free diffusion in the gel of antigens and antibodies in the zone of their optimal ratio, specific complexes are formed - precipitation bands, which are detected visually or by staining. A feature of the method is that each antigen-antibody pair forms an individual precipitation band, and the reaction does not depend on the presence of other antigens and antibodies in the system under study.
1. Put an approximate agglutination reaction on the glass. To do this, a drop of diagnostic serum and a drop of physiological saline are applied to a glass slide with a pipette. A small amount of bacterial culture is introduced into each sample using a bacteriological loop and emulsified. After 2-4 minutes, in a positive case, flakes appear in the serum sample, in addition, the drop becomes transparent. In the control sample, the drop remains uniformly turbid.
2. Set up a detailed agglutination reaction. To set up the reaction, take 6 test tubes. The first 4 tubes are experimental, 5 and 6 are control. 0.5 ml of saline is added to all tubes except 1. In the first 4 test tubes, titrate the test serum (1:50; 1:100; 1:200; 1:400). Add 0.5 ml of antigen to all tubes, except for the 5th one. Shake the tubes and place in a thermostat (37 0 C) for 2 hours, then leave the samples at room temperature for 18 hours. The results are recorded according to the following scheme:
Complete agglutination, well-defined flocculent sediment, transparent supernatant
Incomplete agglutination, pronounced sediment, slightly turbid supernatant
Partial agglutination, there is a small sediment, the liquid is cloudy
Partial agglutination, the sediment is weakly expressed, the liquid is turbid
No agglutination, no sediment, cloudy liquid.
3. Familiarize yourself with the formulation of the precipitation reaction in the diagnosis of a toxigenic strain of C.diphtheriae.
4. Analyze the schemes of direct and indirect Coombs reactions.
Control questions
1. Immunity, its types
2. Central and peripheral organs of immunity. Functions, structure.
3. The main cells involved in immune responses.
4. Classification of antigens, properties of antigens, properties of haptens.
5. Antigenic structure of a bacterial cell, virus.
6. Humoral immunity: features, main cells involved in humoral immunity.
7. B-lymphocytes, cell structure, phases of maturation and differentiation.
8. T-lymphocytes: cell structure, phases of maturation and differentiation.
9. Three-cell cooperation in the immune response.
10. Classification of immunoglobulins.
11. The structure of immunoglobulin.
12. Incomplete antibodies, structure, significance.
13. Reactions of immunity, classification.
14. Agglutination reaction, staging options, diagnostic value.
15. Coombs reaction, formulation scheme, diagnostic value.
16. Precipitation reaction, formulation options, diagnostic value.
resistance (from lat. resistere - resist, resist) - the body's resistance to the action of extreme stimuli, the ability to resist without significant changes in the constancy of the internal environment; this is the most important qualitative indicator of reactivity;
Nonspecific resistance is the resistance of an organism to damage (G. Selye, 1961), not to any individual damaging agent or group of agents, but to damage in general, to various factors, including extreme ones.
It can be congenital (primary) and acquired (secondary), passive and active.
Congenital (passive) resistance is determined by the anatomical and physiological characteristics of the organism (for example, the resistance of insects, turtles, due to their dense chitinous cover).
Acquired passive resistance occurs, in particular, with serotherapy, blood replacement transfusion.
Active non-specific resistance is determined by protective and adaptive mechanisms, arises as a result of adaptation (adaptation to the environment), training to a damaging factor (for example, increased resistance to hypoxia due to acclimatization to a high-altitude climate).
Nonspecific resistance is provided by biological barriers: external (skin, mucous membranes, respiratory organs, digestive apparatus, liver, etc.) and internal - histohematic (hematoencephalic, hematoophthalmic, hematolabyrinthic, hematotesticular). These barriers, as well as biologically active substances contained in fluids (complement, lysozyme, opsonins, properdin) perform protective and regulatory functions, maintain the optimal composition of the nutrient medium for the organ, and help maintain homeostasis.
FACTORS REDUCING NON-SPECIFIC RESISTANCE OF THE ORGANISM. WAYS AND METHODS TO INCREASE AND STRENGTHEN IT
Any effect that changes the functional state of regulatory systems (nervous, endocrine, immune) or executive (cardiovascular, digestive, etc.) leads to a change in the reactivity and resistance of the body.
There are known factors that reduce nonspecific resistance: mental trauma, negative emotions, functional inferiority of the endocrine system, physical and mental overwork, overtraining, starvation (especially protein), malnutrition, lack of vitamins, obesity, chronic alcoholism, drug addiction, hypothermia, colds, overheating, pain trauma, detraining of the body, its individual systems; physical inactivity, a sudden change in the weather, prolonged exposure to direct sunlight, ionizing radiation, intoxication, past illnesses, etc.
There are two groups of ways and methods that increase nonspecific resistance.
With a decrease in vital activity, loss of the ability to independent existence (tolerance)
2. Hypothermia
3. Ganglion blockers
4. Winter hibernation
While maintaining or increasing the level of vital activity (SNPS - a state of non-specifically increased resistance)
1 1. Training of the main functional systems:
physical training
hardening to low temperatures
Hypoxic training (adaptation to hypoxia)
2 2. Changing the function of regulatory systems:
Autogenic training
verbal suggestion
Reflexology (acupuncture, etc.)
3 3. Non-specific therapy:
Balneotherapy, spa therapy
Autohemotherapy
Protein therapy
Non-specific vaccination
Pharmacological agents (adaptogens - ginseng, eleutherococcus, etc.; phytocides, interferon)
To the first group include influences with the help of which stability is increased due to the loss of the body's ability to independent existence, a decrease in the activity of vital processes. These are anesthesia, hypothermia, hibernation.
When an animal in a state of hibernation is infected with plague, tuberculosis, anthrax, diseases do not develop (they occur only after it wakes up). In addition, resistance to radiation exposure, hypoxia, hypercapnia, infections, and poisoning increases.
Anesthesia contributes to an increase in resistance to oxygen starvation, electric current. In a state of anesthesia, streptococcal sepsis and inflammation do not develop.
With hypothermia, tetanus and dysentery intoxication are weakened, sensitivity to all types of oxygen starvation, to ionizing radiation decreases; increases resistance to cell damage; allergic reactions are weakened, the growth of malignant tumors slows down in the experiment.
Under all these conditions, a deep inhibition of the nervous system occurs and, as a result, of all vital functions: the activity of regulatory systems (nervous and endocrine) is inhibited, metabolic processes are reduced, chemical reactions are inhibited, the need for oxygen decreases, blood and lymph circulation slows down, temperature decreases. body, the body switches to a more ancient metabolic pathway - glycolysis. As a result of the suppression of the processes of normal vital activity, the mechanisms of active defense are also turned off (or slowed down), an unreactive state arises, which ensures the survival of the body even in very difficult conditions. At the same time, he does not resist, but only passively endures the pathogenic action of the environment, almost without reacting to it. Such a state is called portability(increased passive resistance) and is a way for the organism to survive in adverse conditions, when it is impossible to actively defend itself, it is impossible to avoid the action of an extreme stimulus.
To the second group include the following methods of increasing resistance while maintaining or increasing the level of vital activity of the organism:
Adaptogens are agents that accelerate adaptation to adverse influences and normalize stress-induced disturbances. They have a wide therapeutic effect, increase resistance to a number of factors of a physical, chemical, biological nature. The mechanism of their action is associated, in particular, with their stimulation of the synthesis of nucleic acids and proteins, as well as with the stabilization of biological membranes.
By using adaptogens (and some other drugs) and adapting the body to the action of adverse environmental factors, it is possible to form a special state non-specifically increased resistance - SNPS. It is characterized by an increase in the level of vital activity, the mobilization of active defense mechanisms and functional reserves of the body, and increased resistance to the action of many damaging agents. An important condition for the development of SNPS is a dosed increase in the strength of the impact of adverse environmental factors, physical exertion, the exclusion of overloads, in order to avoid the disruption of adaptive-compensatory mechanisms.
Thus, the organism that is better, more actively resists (SNPS) or less sensitive and has greater tolerance is more resistant.
Managing the reactivity and resistance of the body is a promising area of modern preventive and curative medicine. Increasing nonspecific resistance is an effective way of general strengthening of the body.
1. One of the determining factors involved in the development of infection and, accordingly, infectious diseases, is an susceptible microorganism. The set of mechanisms that determine the immunity (resistance) of an organism to the action of any microbial agent, denoted by the term "antimicrobial (antimicrobial) resistance". This is one of the manifestations of the general physiological reactivity of the macroorganism, its reaction to a kind of irritant - a microbial agent.
Antimicrobial resistance is purely individual, its level is determined by the genotype of the organism, age, living and working conditions, etc.
An increase in a wide range of nonspecific protection factors, in particular, is facilitated by earlier attachment to the breast and breastfeeding.
By specificitymechanisms of antimicrobial protection are divided:
- on the non-specific - the first level of protection against microbial agents;
-specific - second level of protection provided by the immune system. Implemented in the following way:
Through antibodies humoral immunity;.
Through the function of effector cells (T-killers and macrophages) - cellular immunity.
The first and second levels of protection are closely related through macrophages.
Nonspecific and specific antimicrobial defense mechanisms can be tissue(associated with cells) and humoral.
2.Nonspecific microbial resistance- it innate property of the macroorganism, ensured inherited by quite numerous mechanisms, which are divided into the following types:
- tissue;
humoral;
excretory (functional).
To tissue mechanisms of nonspecific natural antimicrobial defenserelate:
Barrier function of the skin and mucous membranes;
Colonization resistance provided by normal microflora;
Inflammation and phagocytosis (may also be involved in specific defenses);
Barrier-fixing function of lymph nodes;
Areactivity of cells;
The function of natural killers.
The first barrier to the penetration of microbes into the internal environment of the body are leather and mucous membranes. Healthy intact skin and mucous membranes are impervious to most microorganisms. However, some types of pathogens of infectious diseases are able to pass through them. Such pathogens are called especially dangerous these include pathogens of plague, tularemia, anthrax, some mycoses and viral infections. Work with them is carried out in special protective suits and only in specially equipped laboratories.
In addition to a purely mechanical function, the skin and mucous membranes have antimicrobial action - bacteria applied to the skin (for example, E. coli) die fairly quickly. Bacteria in the skin and mucous membranes provide:
Its normal microflora (function of colonization resistance);
Secrets of sweat (lactic acid) and sebaceous (fatty acids) glands;
Lysozyme of saliva, lacrimal fluid, etc.
If the pathogen overcomes the mucocutaneous barrier, then it enters the subcutaneous tissue / submucosal layer, where it is realized one of the main non-specific tissue defense mechanisms - inflammation.As a result of the development of inflammation,:
Delimitation of the source of reproduction of the pathogen from the surrounding tissues;
Its delay at the site of implementation;
Deceleration of reproduction;
Ultimately - his death and removal from the body.
3. During the development of inflammation, another universal tissue mechanism of nonspecific protection - phagocytosis.
The phenomenon of phagocytosis was discovered and studied by the great Russian scientist I. I. Mechnikov.
The result of these many years of work is phagocytic theory of immunity, for the creation of which Mechnikov was awarded the Nobel Prize.
Phagocytic defense mechanism is made up of several consecutive phases:
Recognition;
Attraction;
Absorption;
Killing;
intracellular digestion.
Phagocytosis with all stages is called completed. If the phases of killing and intracellular digestion do not occur, then phagocytosis becomes unfinished. With incomplete phagocytosis, microorganisms remain inside leukocytes and, together with them, are carried throughout the body. Thus, incomplete phagocytosis instead of a defense mechanism turns into its opposite, helping microorganisms to protect themselves from the effects of a macroorganism and spread in it.
Tissue and humoral mechanisms of nonspecific resistance
1. Barrier function of the lymph nodes
2. Other tissue mechanisms of antimicrobial defense
3. Humoral mechanisms of nonspecific resistance
1. If microorganisms break through the inflammatory barrier, i.e. inflammation as a non-specific defense mechanism does not work, then pathogens enter the lymphatic vessels, and from there to the regional lymph nodes. Barrier-fixing function of the lymph nodes implemented as follows:
On the one hand, the regional lymph nodes retain microorganisms purely mechanically;
On the other hand, they provide enhanced phagocytosis.
2. To tissue mechanisms of nonspecific antimicrobial protection are also reactivity of cells and tissuesandactivity of natural killer (NK-cells), which exhibit their properties if the pathogen, breaking through the lymphatic barrier, enters the bloodstream.
3. To the humoral mechanisms of natural non-specific antimicrobial defense relate enzyme systems contained in the blood and other body fluids:
Complement system (may also be involved in specific defense). Complement - this is a non-specific enzymatic blood system, which includes 9 different protein fractions adsorbed in the process of cascade attachment on the antigen-antibody complex and has a lysing effect on antibody-bound cellular antigens. Complement is unstable, it is destroyed by heating, storage, exposure to sunlight;
lysozyme - a protein found in blood, saliva, tear and tissue fluid. It is active against gram-positive bacteria, as it disrupts the synthesis of murein in the bacterial cell wall;
beta lysines - more active against gram-negative bacteria;
leukins - proteolytic enzymes released during the destruction of leukocytes. They violate the integrity of the surface proteins of microbial cells;
interferon- a product of cells with antiviral and regulatory activity;
properdin system- a complex of proteins with antiviral, antibacterial activity in the presence of magnesium salts;
erythrin.
To the excretory (functional) mechanisms of nonspecific natural antimicrobial protectionrelate:
sneezing;
Excretory function of the kidneys and intestines;
Fever.
Protection against microorganisms is not the main function of these mechanisms, but their contribution to the release of the body from them is quite high.
All numerous of the above mechanisms of natural non-specific antimicrobial protection always active against any microbial agents: the activity of these mechanisms does not become more pronounced with repeated or repeated contact with microorganisms. In this way, the mechanisms of nonspecific antimicrobial protection differ from the mechanisms of specific antimicrobial resistance included in immunity.
Nonspecific resistance is carried out by cellular and humoral factors that closely interact in achieving the final effect - the catabolism of a foreign substance: macrophages, neutrophils, complement and other cells and soluble factors.
The humoral factors of nonspecific resistance include leukins - substances derived from neutrophils that exhibit a bactericidal effect against a number of bacteria; erythrin - a substance derived from erythrocytes, bactericidal against diphtheria bacillus; lysozyme - an enzyme produced by monocytes, macrophages, lyses bacteria; properdin - a protein that provides bactericidal, virus-neutralizing properties of blood serum; beta-lysins are bactericidal factors of blood serum secreted by platelets.
Nonspecific resistance factors are also the skin and mucous membranes of the body - the first line of defense, where substances that have a bactericidal effect are produced. Saliva, gastric juice, digestive enzymes also inhibit the growth and reproduction of microbes.
In 1957, the English virologist Isaacs and the Swiss virologist Lindenmann, studying the phenomenon of mutual suppression (interference) of viruses in chicken embryos, refuted the connection between the interference process and competition between viruses. It turned out that the interference is due to the formation in the cells of a specific low molecular weight protein substance, which was isolated in its pure form. Scientists called this protein interferon (IFN) because it suppressed the reproduction of viruses, creating a state of resistance in cells to their subsequent reinfection.
Interferon is formed in cells during a viral infection and has a well-defined species specificity, that is, it manifests its effect only in the organism in whose cells it was formed.
When the body encounters a viral infection, it is the production of interferon that is the most rapid response to infection. Interferon forms a protective barrier on the way of viruses much earlier than the specific protective reactions of the immune system, stimulating cellular resistance, making cells unsuitable for virus reproduction.
In 1980, the WHO Expert Committee adopted and recommended a new classification, according to which all human interferons are divided into three classes:
- alpha-interferon (leukocyte) - the main drug for the treatment of viral and cancerous diseases. It is obtained in the culture of blood leukocytes of donors, using viruses that do not pose a danger to humans (Sendai virus) as interferonogens;
- beta-interferon - fibroblastic, produced by fibroblasts, in this type of interferon, antitumor activity prevails over antiviral;
- gamma-interferon - immune, produced by sensitized T-type lymphocytes upon repeated encounter with an antigen "known" to them, as well as upon stimulation of leukocytes (lymphocytes) by mitogens - PHA and other lectins. It has a pronounced immunomodulatory effect.
All interferons differ from each other in a set of amino acids and antigenic properties, as well as in the severity of certain forms of biological activity. The following properties of interferons are described: antiviral, immunomodulating, antitumor; in addition, interferons inhibit cell growth, change the permeability of cell membranes, activate macrophages, increase the cytotoxicity of lymphocytes, activate the subsequent synthesis of interferon, and also have a "hormone-like" activation of cell vital activity.
In all links of the interaction of the components of the immune system, both at the level of formation, activation and manifestation of their functions, there are many blank spots in order to create a working scheme of the immune system and, on this basis, to predict the development of further events in the body.
