Type I allergic reaction is a rapid reaction (type I allergic reaction), also known as allergic reaction.
The allergen enters the body and induces the production of IgE antibodies by B cells, which have a high affinity for the target cells and are firmly attached to the surface of mast cells and basophils. When the same antigen re-enters the sensitized organism and binds to IgE antibodies, it triggers a series of biochemical reactions in the cell membrane, initiating two processes that occur in parallel: degranulation and synthesis of new mediators. (i) mast cells and basophils produce degranulation changes, releasing many active mediators from the granules, such as histamine, protein hydrolase, heparin, chemokines, etc.; (ii) at the same time, cell membrane phospholipids are degraded, releasing arachidonic acid. It is metabolized in two pathways, synthesizing prostaglandins, thromboxane A2; and leukotrienes (LTs) and platelet-activating factor (PAF), respectively. Various mediators are dispersed throughout the body with blood flow and act on skin, mucous membrane, respiratory tract and other effector organs, causing small vessel and capillary dilation, increased capillary permeability, smooth muscle contraction, increased glandular secretion, eosinophilia and infiltration, which can cause skin and mucous membrane allergies (urticaria, eczema, angioneurotic edema), respiratory tract allergic reactions (allergic rhinitis, bronchial asthma, laryngeal edema) The allergic reactions of the gastrointestinal tract (food allergic gastroenteritis), systemic allergies (anaphylaxis), Summary: Since IgE is mostly secreted by mucous membranes, type I mostly causes mucosal reactions.
Type II allergic reactions i.e. cytotoxic type (type II allergic reactions)
Antibodies (mostly IgG, a few IgM, IgA) first combine with the antigenic components of the cell itself or adsorbed on the membrane surface, and then kill the target cells through four different pathways.
(1) Antibody- and complement-mediated cytolysis: IgG/IgM class antibodies bind specifically to antigens on target cells and then activate the complement system through the classical pathway, finally forming a membrane attack unit, causing membrane damage and thus target cell lysis and death.
(2) Recruitment and activation of inflammatory cells: complement activation produces allergenic toxins C3a and C5a that are chemotactic for neutrophils and monocytes. These two types of cells have IgG Fc receptors on their surface, so IgG binds to them and activates them. Activated neutrophils and monocytes produce hydrolases and cytokines, etc. thereby causing cell or tissue damage.
(3) Immunomodulatory effects: IgG antibody Fc fragment bound to antigen on the surface of target cells binds to Fc receptors on the surface of macrophages, and C3b promotes phagocytosis of target cells by macrophages.
(4) Antibody-dependent cell-mediated cytotoxicity: the Fc segment of the antibody bound on the surface of target cells binds to Fc receptors on NK cells, neutrophils, and monocytes-macrophages, activating them to exert extracellular non-phagocytic killing effects and causing destruction of target cells.
Type III metaplasia i.e. immune complex type (type III metaplasia)
During the immune response, the formation of antigen-antibody complexes is a common phenomenon, but most of them can be cleared by the body’s immune system. If a large number of complexes are deposited in the tissues due to certain factors, it causes tissue damage and the associated immune complex disease.
Several factors influence immune complex deposition as follows.
(1) Size of circulating immune complexes: This is a major factor. In general, medium-sized soluble immune complexes with a molecular weight of about 1000 kD and a sedimentation coefficient of 8.5-19S are easily deposited in tissues.
(2) The ability of the body to clear immune complexes: it is inversely proportional to the degree of deposition of immune complexes in tissues.
(3) Physicochemical properties of antigens and antibodies: if the antigens in the complex are positively charged, then such complexes can easily bind to negatively charged components of the glomerular basement membrane and thus be deposited on the basement membrane.
(4) Anatomical and hemodynamic factors: are important in determining the location of complex deposition. The capillaries in the glomerulus and synovium are overfiltered through the capillary wall under high hydrostatic pressure, making them one of the most frequent sites of complex deposition.
(5) The role of inflammatory mediators: active mediators increase vascular permeability and increase the deposition of complexes in the vessel wall.
(6) Relative ratio of antigen to antibody: complexes with excess antibody or mild antigen excess are rapidly deposited locally at the site of antigen entry.
Common type III allergic diseases include Arthus reaction, primary serum disease, glomerulonephritis after streptococcal infection, etc.
Type IV allergic reactions i.e. late type (type IV allergic reaction)
Unlike the above three types of allergic reactions mediated by specific antibodies, type IV is mediated by specific sensitizing effector T cells. The local inflammatory changes in this type of reaction appear slowly, and the peak reaction occurs only after 24-48 h of exposure to antigen, so it is called delayed-onset metaplasia. After initial exposure to the antigen, T cells are converted into sensitized lymphocytes, leaving the organism in an allergic state. When the same antigen enters again, the sensitized T cells recognize the antigen, differentiate and proliferate, and release many lymphokines, which attract, aggregate and form an inflammatory reaction mainly with monocyte infiltration, and even cause tissue necrosis. Common type IV allergic reactions include contact dermatitis, transplant rejection, and type IV allergic reactions during infection with a variety of bacteria and viruses (such as Mycobacterium tuberculosis and measles virus).
In parasites, Leishmania protozoa cause skin nodules with significant cellular reactions and granuloma formation. When exposed to the antigen again, the sensitized T lymphocytes release lymphotoxin (LT), macrophage movement inhibitory factor (MIF), and eosinophil chemotactic factor (ECF-A), resulting in granulomas with lymphocyte, macrophage, and eosinophil infiltration around the eggs. The granuloma is mainly infiltrated by lymphocytes, macrophages and eosinophils. In parasitic infections, some parasitic diseases may have multiple metaplasia and the pathological consequences are a complex and variable effect of multiple immunopathological mechanisms. As already mentioned, schistosome infections cause caecal dermatitis (type I and IV metaplasia), ADCC effects on child worm killings (type II metaplasia), schistosome glomerulonephritis (type III metaplasia), and schistosome egg granuloma (type IV metaplasia). Another example is the insect-induced metaplasia, which is mainly rapid and delayed, and partly of the immune complex type. When an insect bites, its secretions, excretions and toxic hairs (allergens) invade the body and induce local and systemic metabolic reactions.
Parasitic infections are summarized below.
Examples of fractional immune component damage mechanisms parasitic infections
IIgE mast cells, basophils and their mediators schistosome larvae dermatitis, tropical pulmonary eosinophilia, shock due to rupture of encysted worms
IIIgM,IgG complement activation, leukocyte chemotaxis, activation, NK cell action malaria (three-day malaria) anemia, Chagas disease myocarditis
IIICAg complement activation, leukocyte chemotaxis, activation malaria (three-day malaria) nephrotic syndrome, acute schistosomiasis
IVCD8+ T cellsCD4+ T cells direct target cell lysis, activated phagocytosis, cytokine release leading to inflammatory cutaneous leishmaniasis, schistosomiasis caecalis dermatitis, cirrhosis, filarial elephantiasis