Circulating immune complexes. Great encyclopedia of oil and gas
Like autoimmunity (page 25), the formation of antigen-antibody complexes or immune complexes (ICs) is normal physiological process, aimed at protecting the body from potentially pathogenic influences. However, under certain conditions, IR can play an important role in the development of rheumatic diseases. Classic manifestations of the immune complex process associated with impaired clearance and deposition of IR in tissues are vasculitis, nephritis and arthritis, which are among the leading forms of organ pathology in many cases. rheumatic diseases. In rheumatic diseases, the development of immune complex pathology is associated with the following factors: 1. Disruption of the mechanisms of normal clearance of immune complexes from bloodstream: a) genetically determined (p. 81), or acquired pathology of the complement system, leading to disruption of the process of inhibition of immune precipitation and solubilization of antigen-antibody complexes, which promotes the circulation of complexes with a more pronounced inflammatory potential and the possibility of their deposition in target organs; b) congenital or acquired impairment of erythrocyte clearance of immune complexes due to pathology of CR1 erythrocyte receptors; Recently, a violation of the expression of CR1 receptors on the erythrocytes of patients with antiphospholipid syndrome was shown (p. 13): c) blockade functional activity Fc receptors of mononular phagocytic cells localized in the liver and spleen. 2. Overproduction of circulating immune complexes with a certain structure and charge, which have the ability to bind to charged biomolecules of target organs. Recently, it was shown that in SLE, the formation of anti-DNA containing IR expressing idiotypes 0-81 correlates with SLE activity and the development of diffuse proliferative nephritis with subendothelial deposits. Overproduction of IR containing IgM and IgG RF correlates with the development of rheumatoid vasculitis. Cryoprecipitating immune complexes can play a particularly important pathogenetic role (p. 95).
In general, in systemic rheumatic diseases, autoimmune and immune complex pathological processes are in close relationship, which is determined by a common genetic predisposition to impaired immunoregulation and weakened clearance of immune complexes and similar mechanisms of inflammation and tissue destruction mediated by autoantibodies and immune complexes.
Clinical significance of determining circulating immune complexes (CIC).
To determine the CEC, it is advisable to use several methods based on different principles: 1. C1q binding method.
Changes in the concentration of CEC, determined by the C1q binding method, correlate with the articular index in RA and, in some cases, with the activity of the pathological process in SLE. However, this method may produce false-positive results due to the production of antibodies to C1q, especially when used for the detection of solid-phase immobilized CEC C1q.
2. Method using Raji cells.
Until recently, this method was considered as the most sensitive way to detect CEC.
TO The disadvantages of this method include the possibility false positive results due to binding
With antilymphocyte antibody cells. (p. 103), often present in serums patients with SLE. This method is sometimes used to assess disease activity in systemic necrotizing vasculitis and sarcoidosis.
3. Method of precipitation of immune complexes with polyethylene glycol.(PEG method).
The simplest and most frequently used method for determining CEC in clinical practice: an increase in the concentration of CEC according to this method correlates with the inflammatory and immunological activity of the process in SLE and RA. seronegative arthropathy. The disadvantages of the method include its insufficiently high sensitivity, difficulties in quantitatively assessing the content of CEC in terms of aggregated gammaglobulin, and the dependence of the results on the concentration of IgG in the serum. 4. IgA-containing CECs.
Detection of IgA-containing immune complexes correlates with hematuria in ankylosing spondylitis, in which IgA nephropathy can develop. IgA-fibronectin complexes are most characteristic of IgA nephropathy, while they are not detected in ankylosing spondylitis. The formation of C1q-binding immune complexes and IgA-containing immune complexes correlates with seropositivity, disease activity, and the development of vasculitis in RA. 5. Composition of circulating immune complexes. Exogenous or endogenous antigens can be found in the CEC - yersinia in yersinia arthritis, HBsAg in urticarial vasculitis and periarteritis nodosa, DNA in SLE. Antibodies to Borrelia burgdorferi are present in the CEC in seronegative patients with Lyme borreliosis.
It is assumed that in autoimmune diseases, in which it is rarely possible to detect any autoantigen in the immune complexes, the formation of idiotipantiidiotypic immune complexes, the production of which is associated with polyclonal B-cell activation, is of primary importance.
LITERATURE.
Nasonov E.L. Immune complexes in rheumatic diseases. Results of science and technology. Immunology Series, Volume II, 1984, pp. 104-158; Nasonov E.L., Sura V.V. The relationship between autoimmune and immune complex pathologies: current state problems Therapist. archive, 1984, No.10, pp. 4-10. Nasonov E. L. Methodological aspects of determining circulating immune complexes using polyethylene glycol. Therapist. archive, 1987, No.4, pp. 38-45; Davies K.A. Immune complexes and disease. Eur. J. Int. Med. 1992; 3:95-108.
INTERMITTING HYDRATHROSIS
A rare disease characterized by recurrent accumulation of fluid in the joint, repeated at regular intervals. Usually the disease is idiopathic in nature, but sometimes similar pathology develops with RA, ankylosing spondylitis or Reiter's syndrome. It differs from palindromic rheumatism (p. 125) in the regularity of attacks and the distribution of joint damage.
It affects men and women with equal frequency and occurs at any age (peak 20-50 years). Clinical manifestations: Usually one or two joints are affected, most commonly the knee (90%); V
In 65% of cases, only the knee joints are involved in the process, and in 60% of patients there is a bilateral process or lesion knee joints observed in different periods illness; in other cases, only one knee joint is affected, sometimes the elbow joint (15%), very rarely the shoulder, ankle, temporomandibular joints, small joints of the hands and feet; during repeated attacks, the same joints are involved in the process; The attack is characterized by the rapid (within 12-24 hours) appearance of effusion in the joint, pain, and limited mobility. On examination, a large effusion in the joint cavity is detected, very rarely low-grade fever; the effusion disappears within 2-6 days, and then reappears after a fixed period of time (3-30 days, especially often on days 10, 14 and 21). The frequency is strictly maintained for each patient. The process can recur over many years, but 60% of patients develop long-term remissions, lasting up to 10 years or more. Deformations usually do not develop.
X-ray examination: expansion of the joint space. sometimes when long term illnesses degenerative changes.
Laboratory examination: ESR is within normal limits, RF is not detected: non-inflammatory synovial fluid: biopsy of the synovial membrane reveals nonspecific synovitis.
Treatment: analgesics, NSAIDs, fluid aspiration, intramuscular injection of GC, as a rule, does not have a significant effect; There is evidence of the effectiveness of gold salts and synovectomy, but this treatment should be reserved only for patients with the most severe course of the disease.
ISCHEMIC BONE DISEASE
A syndrome in which the development of cartilage necrosis and bone tissue associated with circulatory disorders due to inflammation of the vessel (arteritis), thrombosis, embolism, changes external pressure on the vessel wall, injury.
Reasons: 1. Trauma (femoral neck fracture). 2. Arthropathy (RA, psoriatic arthritis, severe osteoarthritis, neuropathic joint). 3. Endocrine and metabolic diseases (treatment with GC, Cushing's disease, alcoholism, gout, osteomalacia). 4. Storage diseases (Gaucher disease (p. 68)). 5. Caisson disease. 6. Systemic rheumatic diseases (SLE), antiphospholipid syndrome(p. 52); giant cell arteritis. 7. Pancreatitis, pregnancy, burns, endocarditis, radiation, polycythemia, electric shock, local administration of GC, Perthes disease (p. 128), Thielman disease (p. 182). 8. Idiopathic avascular necrosis.
Ischemic necrosis often develops in the head hip bones in middle-aged men (age 30-60 years, male to female ratio 4:1), in 30% of cases the lesion is bilateral.
Clinical manifestations: pain of varying degrees of intensity, stiffness in the affected joint, limited mobility, effusion when the knee joint is affected.
X-ray examination: small areas of infarction against the background of sclerosis and osteoporosis, areas of collapse articular surface, necrotic fragments (the picture resembles osteochondritis dissecans,
Laboratory test: changes depend on the underlying disease.
Treatment: in early stage complete immobilization, analgesics; in the late stage, surgical treatment.
KAWASAKI DISEASE
Acute febrile illness childhood, first described in Japan in 1967. The etiology is unknown, however, the epidemiological features and the range of clinical manifestations indicate infectious nature diseases.
The disease is slightly more common in boys than in girls (ratio 1.4:1). The disease mainly affects children under 5 years of age (90%).
Clinical manifestations: 1. High, intermittent fever (1-2 weeks in the absence of treatment). 2. Conjunctivitis with a predominant lesion of the bulbar conjunctiva without pronounced exudation develops following an increase in temperature and persists for 1-2 weeks. 3. Erythema, dryness, peeling and bleeding of the lips, erythema of the tonsils, “crimson” tongue with diffuse erythema and hypertrophy of the papillae. 4. Erythema (or induration of the skin of the palms and soles, accompanied by severe pain, limited mobility, inability to make fine movements (10-20 days from the onset of fever); peeling of the fingers begins from the periungual zone, and then spreads to the palms
And soles. 5. Polymorphic rash (the first 5 days from the onset of fever); urticarial exanthema with large erythematous plaques, macropapular multiforme-like, scarlet-like erythroderma localized on the trunk and limbs, in the perineal area. 6. Single-sided or double-sided cervical lymphadenopathy; On palpation, the lymph nodes are dense and sometimes painful. 7. Unusually high excitability, more pronounced than in other febrile diseases in children. 8. Joint damage (30%): arthralgia or polyarthritis of the knees, ankle joints and small joints of the hands (develops during the first week, persists for about 3 weeks). 9. Damage to the cardiovascular system (45%): heart murmur, tachycardia, gallop rhythm, cardiomegaly, prolongation of the PQ interval and widening of the QT complex, decreased voltage, ST segment depression, arrhythmia; with coronary angiography
And echocardiographic examination reveals aneurysms, narrowing, and obstruction of blood vessels; the development of myocardial infarction is described, usually during the first year of the disease, in 30% of asymptomatic patients.
The first 5 signs occur in more than 90% of patients, and 6 - in 50-75% (enlargement of at least one lymph node by more than 1.5 cm) relate to the diagnostic criteria of the disease. 5 out of 6 signs are required to make a diagnosis.
Laboratory examination: leukocytosis, neutrophilia, increased ESR, thrombocytosis, increased concentration of C-reactive protein, urine tests - proteinuria and leukocyturia. Diagnostic criteria Kawasaki disease (p. 249). Treatment: aspirin at a dose of 80-120 mg/kg per day ( acute phase illness until C-reactive protein normalizes, then the dose is reduced to 30 mg/kg per day until ESR normalizes; maintenance dose during convalescence 3-5 mg/kg/day; intravenous immunoglobulin 400 mg/kg/day for 5 days (preferably in the first 10 days from the onset of illness).
LITERATURE.
Wortmann DW, Nelson AM. Kawasaki syndrome. Rheumatic Disease Clinic North. Amer. 1990; 16:363-375.
CALPROTECTIN
A non-glycosylated protein that makes up 60% of the soluble proteins of the cytosolic fraction of neutrophil granulocytes, which is released from cells during the period of their activation and destruction. Calprotectin has calcium-binding and antimicrobial activity. An increase in serum calprotectin concentrations is observed in various infectious and chronic inflammatory diseases, including RA and SLE. In RA, serum calprotectin levels correlate with CRP concentrations, ESR and clinical activity parameters, as well as detection of RF. In SLE, calprotectin concentrations correlate with disease activity, anti-DNA antibody levels, and the development of arthritis. It is assumed that the level of calprotectin may be a new laboratory indicator of the activity of the pathological process in rheumatic diseases.
CARCINOID SYNDROME
Rare syndrome associated with the production of 5-hydroxytryptamine and other biologically active amines
carcinoid tumor, which originates from argentophilic cells of the small intestine. Occasionally, against the background of the disease, transient arthritis develops, characterized by symmetrical damage to the interphalangeal joints of the hands with severe swelling and pain, sometimes flexion contractures. A characteristic manifestation of the syndrome is a sharp reddening of the face, with subsequent development of persistent erythema and telangiectasia, weight loss, chronic diarrhea, asthmatic attacks, liver enlargement, tricuspid and valve damage pulmonary artery hearts. The diagnosis is confirmed by the detection of increased urinary excretion of 5-hydroxytryptamine.
KASHIN-BEK DISEASE (level disease)
An endemic disease based on disorders of enchondral ossification, leading to the development of multiple deforming osteoarthritis. The disease occurs in Eastern Siberia, Northern China, North Korea. The etiology is not clear; exogenous factors characteristic of the corresponding endemic zones are of undoubted importance.
It occurs with equal frequency in men and women and begins in childhood and adolescence. Clinical manifestations: Damage to small joints of the hands, wrists, ankles, knees, hip joints, then the spine. On examination, joint pain, swelling, stiffness, limited mobility, crepitus, and inflammatory changes are absent; later, severe deformation and shortening of the fingers, reminiscent of arthritis mutilans, may develop. The course is chronic, slowly progressive, leading to complete disability.
X-ray examination: degenerative changes in the form of narrowing of joint spaces, sclerosis, cystic clearings; for more late stages- bone destruction, especially of the phalanges of the fingers.
Laboratory examination: no pathology is detected. Treatment: analgesics, NSAIDs.
KIKUCHI DISEASE (histiocytic necrotizing lymphadenitis)
Disease; manifested by painless, unilateral cervical lymphadenopathy, later generalized involvement of the lymph nodes (20%), fever, weakness, skin lesions like urticaria, occasionally splenomegaly, enlarged mesenteric lymph nodes simulating appendicitis; laboratory tests reveal neutropenia, lymphocytosis, a sharp increase in ESR, and an increase in the concentration of liver enzymes; During immunological examination, antibodies to DNA (p. 70) and antilymphocyte antibodies (p. 103) are detected in the sera of patients. Usually the disease ends with spontaneous recovery within 3 months, less often it persists for up to a year. At histological examination lymph nodes reveal patchy paracortical (T zone) necrosis, consisting of eosinophilic fibrinoid material containing large number nuclear fragments, the necrosis zone is surrounded by histiocytes, macrophages, T cells in the absence of plasma cells and polymorphonuclear leukocytes.
Kikuchi disease is thought to be a benign lupus-like syndrome associated with infection with parvovirus B19; The development of characteristic clinical and pathomorphological signs of pathology in classical SLE and Still's disease is described. Treatment: prednisolone 1 mg/kg/day (relieves constitutional symptoms and fever).
LITERATURE.
Meyer OS. Kikuchi's disease revisited. Clin. Exp. Rheumatol. 1992; 10:1-2.
CLUTTON JOINTS
Bilateral hydrarthrosis of the knee joints, developing with secondary syphilis. This disease is sometimes misdiagnosed as Still's disease.
This form of articular pathology occurs with equal frequency in men and women, and develops at the age of 8-15 years in 10% of patients with congenital syphilis.
Clinical manifestations: 1. Asymmetrical involvement of the knee joints (damage to one joint often precedes damage to the other joint by several years; very rare pathological process develops in the ankle and elbow joints. The disease begins gradually with joint pain
Diseases with the presence of immune complexes
There are pathological processes in the pathogenesis of which immune complexes (IC) take part, i.e. connection of an antibody with an antigen. In principle, this process is a normal mechanism for removing antigen from the body. However, in some cases it may be the cause of the disease. There are immune complexes various types: with low molecular weight (they are easily excreted from the body in the urine), large, which are successfully captured by phagocytes and destroyed, but sometimes this process leads to the release of proteolytic enzymes and bioactive substances that damage tissue from phagocytic cells. And finally, medium-weight IR, which can thrombose capillaries, bind to complement and cause organ damage. The body has a special self-control system that limits the pathogenic effect of IR on tissue and is disrupted only in various pathologies. In general terms, the formation of IC in the circulation triggers a cascade of complement activation, which in turn solubilizes IR, i.e. transfers the insoluble immune precipitate of AG-ATs into a dissolved state, reduces their size and converts them into ICs that have lost
its biological activity. Such ICs are also called “dead-end”. In this regard, it can be assumed that one of the essential functions complement in the body is to prevent the formation of large IC. Apparently, therefore, the formation of IR in healthy body quite difficult.
Diseases with the presence of immune complexes are the following.
1. Idiopathic inflammatory diseases: SLE, RA, ankylosing spondylitis, essential cryoglobulinemia, scleroderma.
2. Infectious diseases:
a) bacterial streptococcal, staphylococcal, subacute endocarditis, pneumococcal, mycoplasma, leprosy;
b) viral - hepatitis B, acute and chronic hepatitis, Dengue fever, infectious mononucleosis, CMV - disease of newborns;
3. Kidney diseases: acute glomerulonephritis, IgA nephropathy, kidney transplant.
4. Hematological and neoplastic diseases: acute lymphoblastic and myeloblastic leukemia; chronic lymphocytic leukemia; Hodgkin's disease; solid tumors affecting the lungs, chest, colon; melanoma, severe hemophilia, immune hemolytic anemia, systemic vasculitis.
5. Skin diseases: dermatitis herpetiformis, pemphigus and pemphigoid.
6. Diseases gastrointestinal tract: Crohn's disease, ulcerative colitis, chronic active hepatitis, primary biliary cirrhosis.
7. Neurological diseases: subacute sclerosing panencephalitis, amyotrophic lateral sclerosis.
8. Diseases endocrine system: Hoshimoto's thyroiditis, juvenile diabetes.
9. Iatrogenic diseases: acute serum sickness, D-penicillin nephropathy, drug-induced thrombocytopenia.
As can be seen from the presented list compiled by E. Neidiger et al. (1986), not every disease in which immune complexes are detected has elements of autoimmune reactions in its pathogenesis. One example is serum sickness.
On the other hand, diffuse glomerulonephritis and chronic rheumatism are induced by streptococcal infection, in which IR are deposited along the basement membranes of the glomerulus of the renal corpuscle (glomerulonephritis), in the heart tissue (chronic rheumatism). In turn, antibodies against cross-reacting antigens interact with streptococci, myocardial tissue, glycoproteins of heart valves, blood vessel antigens, etc.
Atherosclerosis, endarteritis and other pathological processes are accompanied by the deposition of immune complexes on inner wall vessels, cause their diffuse inflammation.
It should be especially noted that IC belongs to vital role in the development of various systemic vasculitis, which are based on generalized vascular damage with secondary involvement of various organs and tissues in the pathological process. The commonality of their pathogenesis is a violation of immune homeostasis with the uncontrolled formation of autoAb, IC, circulating in the bloodstream and fixing in the wall of blood vessels with the development of a severe inflammatory reaction. This concerns hemorrhagic vasculitis(Henoch-Schönlein disease), when IR containing IgA is deposited in the vascular wall, followed by the development of inflammation, increased vascular permeability, and the appearance of hemorrhagic syndrome. IR is equally important when Wegener's granulomatosis, when the level of serum and secretory IgA increases, IC are formed and fixed in the vascular wall. Periarteritis nodosa According to their pathogenesis, they are also classified as immune complex diseases with complement activation. Typical features of immune complex inflammation are observed. Hemorheological disorders and the development of disseminated intravascular coagulation syndrome are of great importance. Moreover, in the development of internal combustion engines one of the key reasons The primary effect of immune complexes on platelets is also considered. There is an opinion that when serum sickness, SLE, post-streptococcal glomerulonephritis, immune complex damage is responsible for the main clinical manifestations diseases.
Diagnosis of immune complex diseases
Immune complexes are detected different methods in blood or tissues. In the latter case, anti-complementary antibodies labeled with fluorochromes and anti-IgG, IgM, IgA enzymes are used, which detect these substrates in IR.
Treatment of diseases associated with immune complexes
Treatment of diseases associated with immune complexes includes the following approaches.
2. Removal of antibodies: immunosuppression, specific hemosorption, blood cytopheresis, plasmapheresis.
3. Removal of immune complexes: exchange transfusions plasma, hemosorption of complexes.
To this we can add the use of immunomodulators that stimulate the function and motility of phagocytic cells.
As can be seen from these data, immune complex diseases are closely related to autoimmune diseases, often occur simultaneously with them, and are diagnosed and treated in approximately the same way.
Different antigens invade our body every second, but at the same time fall under neutralization immune antibodies. The compounds formed through this interaction are called circulating immune complexes. For the human body, this process is the norm, however, only if antibodies are truly capable of suppressing antigens, while mononuclear phagocytes cause a destructive effect, and also remove the remaining parts of foreign microorganisms from the body.
If there is an excess of antigens in the body, that is, bacteria, infections, viruses that are simply beyond the control of antibodies, then special immune complexes occur. It is they that accumulate in the kidneys, blood vessels, and other parts of our body, while having a destructive effect on them. Such circulating immune complexes have long been recognized main reason occurrence of all systemic autoimmune diseases. Systemic lupus erythematosus, autoimmune hepatitis, endocarditis and even glomerulonephritis are considered the most serious diseases that cause immune complexes, the amount of which in the blood exceeds the norm.
We have already said that the process during which circulating immune complexes are produced is considered normal for the human body. True, only until the body is able to adequately fight antigens. Thus, in order for such immune complexes not to cause harm to the body, a very strong immune system is required, the response of which to the manifestation of antigens could remove them before they cause harm to human health.
Circulating immune complexes in human blood are directly dependent on red blood cells. In this situation, they are practically unable to cause destruction to organs and blood vessels. The most dangerous are the free circulating immune systems present in the blood plasma. The concentration rate is 30-90 IU/ml. As soon as upper limit will be exceeded, it will be possible to report on the development systemic disease in the human body. Let's clarify: the connection has already been established this phenomenon with the occurrence of systemic lupus erythematosus. In addition, this may indicate the development of immune pathology.
Those circulating immune systems, the norm of which is off scale, can come to the surface not only through the blood, but also through other biological fluids. This process indicates that an inflammatory process or even malignancy. Naturally such serious illnesses do not occur after one excess. Only in cases where the indicators are exceeded several times can we talk about the occurrence of such diseases.
Thus, we can conclude that the formation of circulating immune complexes is a kind of game called “roulette”. If today antibodies emerged victorious in the battle with antigens and were able to not only destroy them, but also remove all remains from the body, then tomorrow a stronger antigen may enter our body, which the immune system is simply unable to fight. It turns out that the pathological process is activated. A lot of time can pass between the moment of penetration and the onset of the disease, so we usually understand that we get sick already at the moment the disease grows into our body.
Is it possible not to risk your body? Unfortunately, there is only the only way keep your body in healthy condition. To do this, it is necessary to allow cases of penetration of antigens. Indeed, what could be even simpler and more logical. True, despite all its simplicity, it is very difficult to do this, given that we live in difficult conditions, a polluted aggressive environment
In fact, the problem is whether rapid destruction is awarded to those antigens that are already known to the immune system as “the enemy.” If the immune system does not yet know what it has encountered, then it has to spend time on the formation of circulating immune complexes. There is another development of the current situation. In this case, the antigen will be destroyed instantly, so the body does not have any risk of getting sick.
If you want to help your immune cells get all the information they need about existing antigens, you need to use a drug called Transfer Factor. This medicine is saturated with special chains, which include 44 amino acids. They contain all the required information about antigens that should not be allowed into our body.
This information in medicine is called immune memory. It is present not only in humans, but also in every representative of the mammalian class. Peptide chains, also called transfer factors, are unique formations that contain data that has accumulated over many millions of years. 4Life obtains transfer factors from bovine colostrum. As we know, colostrum is considered an essential component for each mammal, containing the largest number of transfer factors that must be transferred to the child from the mother.
A remedy such as Transfer Factor must be used by every modern person. And all because environment negatively affects the immune system. Transfer factor will allow you to restore all necessary functions immune cells. Anyone can take this remedy, including children, infants, the elderly, and even pregnant women. Many clinical trials and studies have confirmed that Transfer Factor is safe for humans.
Immune complex diseases (type III hypersensitivity) result from tissue deposition soluble complexes antigen-antibody. Which leads to inflammation.
The damage in this type of allergic reaction is caused by AG-AT immune complexes. Reactions constantly occur in the body with the formation of the AG-AT complex. These reactions are an expression of the protective function of the immune system and are not accompanied by damage. But under certain conditions, the AG-AT complex can cause damage and the development of the disease. Immune complexes are formed when there is an excess of antigen and antibodies. The concept that immune complexes (ICs) may play a role in pathology was proposed as early as 1905 by Pirquet and Schick. Since then, a group of diseases in the development of which IR plays a major role began to be called diseases of immune complexes.
Immune complex diseases can be:
* systemic - which are caused by circulating antibodies (for example, serum sickness);
* local - as a result of the formation of immune complexes at the site of penetration of antibodies (for example, the Arthus phenomenon).
There may also be delayed allergic reactions involving Ig G class antibodies, which are also fixed on mast cells with the participation of the C3 component of complement. They are also a manifestation of type 3 hypersensitivity reactions.
The conditions for the development of the immune complex mechanism of immunopathology are:
* presence of long-term (chronic) infectious process, which assumes a constant flow of antigens into the blood;
* predominance of antibody reactions, i.e. the advantage of type 2 T helper cells, which control the development of the humoral immune response;
* relative insufficiency of factors for the destruction and elimination of the CEC from the bloodstream, namely the complement system and the phagocytic reaction of neutrophils and macrophages;
* properties of the CEC. The pathogenic properties of CEC are determined by the totality of their physical and chemical properties, which include size, concentration, composition, solubility, and ability to fix complement. The molecular weight of CECs determines their size, which is the most important indicator pathogenicity. Also, the molecular weight determines the rate of elimination of CECs from the body: large CECs are quickly eliminated and are relatively low-pathogenic; small CECs are poorly eliminated, can be deposited subendothelially, and are not able to activate the complement system; Medium-sized CECs have a high complement-fixing ability and are the most pathogenic.
Immune complexes in type 3 allergic reactions deposited on the vascular wall or on basement membranes Oh. This deposition of immune complexes causes immune complex inflammation. Its essence comes down to the activation of the classical pathway of the complement system with the formation of C3a and C5a complement components. They attract macrophages, neutrophils, mast cells, which determine tissue damage. In addition, intravascular deposits of immune complexes lead to platelet aggregation with the formation of microthrombi, which enhance the accumulation of inflammatory mediators, resulting in the destruction of blood vessels and their replacement with connective tissue.
The following stages are distinguished in the pathogenesis of immune complex reactions:
I. Immunological stage. In response to the appearance of an allergen or antigen, the synthesis of antibodies begins, mainly of the IgM and IgG classes. These antibodies are also called precipitating antibodies for their ability to form a precipitate when combined with the corresponding antigens. When AT combines with AG, IR is formed. They can form locally, in tissues or in the bloodstream, which is determined by the routes of entry or the place of formation of antigens (allergens). The pathogenic significance of IR is determined by their functional properties and the localization of the reactions they cause.
II. Pathochemical stage. Under the influence of IR and in the process of its removal, a number of mediators are formed, the main role of which is to provide conditions conducive to phagocytosis of the complex and its digestion. However, under unfavorable conditions, the process of formation of mediators can be excessive, and then they begin to have a damaging effect.
The main mediators are:
1. Complement, under conditions of activation of which various components and subcomponents have a cytotoxic effect. The leading role is played by the formation of S3, C4, C5, which enhance certain components of inflammation (S3v enhances the immune adhesion of IC to phagocytes, S3 and C4a play the role of anaphylatoxins).
2. Lysosomal enzymes, the release of which during phagocytosis increases damage to basement membranes and connective tissue.
3. Kinins, in particular bradykinin. When the damaging effect of IR occurs, the Hageman factor is activated; As a result, bradykinin is formed from alpha globulins in the blood under the influence of kallikrein.
4. Histamine and serotonin play a large role in type III allergic reactions. Their sources are mast cells, platelets and basophils. They are activated by the C3 and C5a components of complement.
5. Superoxide anion radical is also involved in the development of type III allergic reactions.
All of these mediators enhance proteolysis.
III. Pathophysiological stage. As a result of the action of mediators, inflammation develops with alteration, exudation and proliferation. Vasculitis develops, leading to the appearance of, for example, glomerulonephritis. Cytopenias, such as granulocytopenia, may occur. Due to activation of Hageman factor and/or platelets, intravascular coagulation may occur.
The third type of allergic reactions is leading in the development of serum sickness, some cases of drug and food allergies, in some cases of autoimmune diseases, etc. With significant activation of complement, systemic anaphylaxis develops in the form of shock.
Circulating immune complexes in plasma are evidence of the presence of various inflammatory processes. Thanks to such research, you can find out about the presence of autoimmune diseases and monitor their activity. A doctor can prescribe such a diagnosis if it is impossible to diagnose the patient for certain reasons, but he suspects the presence of autoimmune viral, fungal and other diseases. Analysis of circulating immune complexes is carried out in both adults and children. The study can be performed as a separate procedure or in a group with other blood tests.
CEC are components that begin to be produced by the human body and are formed in the blood as a response to exposure to foreign bodies. Such complexes usually include antigens, antibodies and other elements. If a person does not have an appropriate reaction and the production of the central nervous system is disrupted, then this indicates that a malfunction has occurred in the patient’s body immune system. The main task of such components is to recognize and remove harmful bodies and allergens from the body as quickly as possible. After the CECs have completed their function, they are usually destroyed by phagocytes.
Circulating immune complexes can form not only directly in the blood, but also in the liver. When they are no longer needed, they are removed from the body. If a person is very sick or infected with an infectious disease, then the level of components increases significantly. In this case, they begin to be deposited on the liver and eventually form a dense film, which provokes the formation of an inflammatory process. If such a lesion was not noticed at an early stage, this can lead to the spread of inflammation to other internal organs of the abdominal cavity. Often such changes can lead to cancer. The normal content of CEC in plasma should be 30-90 IU/ml.
When and why is research performed?
The test is usually used to diagnose general condition patient. This is necessary before undergoing a major operation, during pregnancy, or in the presence of cancer. Through such diagnostics it is possible to detect the presence in the body immune pathology or severe allergic reaction.
Chronic infections that are present in the human body may not manifest themselves externally and may not be accompanied by pronounced symptoms, but they can be easily detected during analysis of circulating immune complexes. Such diagnostics make it possible to monitor the development of glomerulonephritis and adjust its treatment. In case of damage to the immune system, a blood test is the best way to monitor the trend of development or cessation of the disease.
Quite often, only such a blood test will allow the doctor to obtain full picture the course of all allergic and viral processes in the body. The analysis is carried out more than once. If the diagnosis is part of a study of the state of the immune system, then the analysis will have to be repeated several times. During the treatment period, the patient does not need to follow a diet or resort to additional measures preparation for analysis. The process of donating blood can be quite painful, but these sensations disappear immediately after the procedure.
The doctor may prescribe such a diagnosis in several cases. Often the cause is an autoimmune pathology in the patient. If a person suspects arthritis, lupus, polymyositis, vasculitis or scleroderma, then this is a reason to conduct a diagnosis. She will be able to confirm or refute the diagnosis. Often such a blood test is prescribed to patients with joint syndromes, defeats cartilage tissue and blood vessels, kidney or liver dysfunction. This analysis is an integral part of the diagnosis when examining the immune system.
Increased rate in patients
In addition to the fact that circulating immune complexes are created by the human body, they are also destroyed by it. Phagocytes begin to influence those bodies that have already completed their protective function, and destroy them. But if the patient has an autoimmune disease, this means that either the body produces too many antibodies at one time, or they are not destroyed after they have completed their task.
If the CEC produces too much, then they lose all their properties. As a result, the human body contains many elements that cannot protect it and at the same time provoke inflammatory processes. Unused or excess circulating immune complexes begin to deposit on human organs. The kidneys suffer the most. They are covered with a layer of elemental cells, and their function is hampered. Inflammation begins, which can lead to the progression of diseases, tissue destruction or partial atrophy of the organ.
Antibody formation - necessary process which must occur in the body. If there is an excess content of complexes and their functioning is disrupted, viruses and allergens can enter the body, which nothing can resist. At this time human body especially susceptible various diseases. Even the simplest ARVI can cause serious damage and transform into another disease.
At increased content In the blood of complexes in the human body, the formation of not only inflammatory processes, but also tumors is observed. Such diseases and neoplasms can lead to the development of pathologies and serious damage to the immune system and all internal organs. In order to conduct the study, you need to take a test of your blood, which will then be combined with C1q elements. The result will depend on how able the plasma cells are to interact with the C1q components.
Element level reduction
A decrease in the number of CECs entails deviations and tissue destruction. Insufficient production of elements provokes diseases of the immune system, since now the body cannot independently protect itself from harmful factors from the outside. If complexes insufficient quantity, then this leads to their accumulation on individual bodies. Substances lose their basic functions and grow on the tissues of the body, while destroying it. This occurs due to cell breakdown and a decrease in the density of vascular walls. As a result, the content of CEC in tissues increases and phagocytes can no longer break them down.
CECs can be found not only independently in the patient’s plasma, but also in association with red blood cells. These links, in excess or deficiency, do not have a destructive effect and do not cause significant harm to the body, therefore, during the study, attention is paid exclusively to the presence of components directly in the patient’s blood.
The level of elements can be checked by reaction to substances C3d and C1g. If the indicators are significantly reduced, then this indicates damage to the gene that is responsible for the transformation of protein elements in the body. Reduced value indicates the presence allergic disease, vasculitis or autoimmune lesion. Often this indicator means the presence of hepatitis, HIV, infectious arthritis or endocrit.
