Allergic diseases and other hypersensitivity reactions: causes, symptoms, diagnosis, treatment

Allergic diseases and other hypersensitivity reactions are the result of an inadequate, overly pronounced, immune response, not corresponding to the severity of the disease or infectious process.

According to the classification of Jell and Kubbs, four types of hypersensitivity reactions are distinguished. Hypersensitivity reactions usually involve several types.

Type I (immediate-type hypersensitivity) is mediated by IgE. The antigen binds to IgE (which joins tissue basophils or blood basophils), triggers the release of finished mediators (such as histamine, proteases, chemotactic factors) and the synthesis of other mediators (such as prostaglandins, leukotrienes, platelet activating factor, IL). These mediators provide vasodilation; increase the permeability of capillaries; lead to hypersecretion of mucus, contraction of smooth muscles, infiltration of tissue with eosinophils, T-lymphocytes of type 2 helper (Th2), and other cells involved in inflammation. Type I reactions underlie atonic disorders (including allergic asthma, rhinitis, conjunctivitis), as well as allergies to latex and certain foods.

Type II arise when the antibody binds to cellular or tissue allergens or haptens connected to cells or tissues.

The antigen-antibody complex activates cytotoxic T-lymphocytes, or macrophages, or a complement system, leading to cellular or tissue damage (antibody-dependent cell-mediated cytotoxicity). Violations related to type II reactions include acute rejection reactions in organ transplantation, Coombs-positive hemolytic anemia, Hashimoto's thyroiditis, Goodpasture's syndrome.

Ill type are due to inflammation in response to circulating antigen-antibody complexes that are deposited in tissues or walls of blood vessels. These complexes can activate the complement system or bind and activate certain immune cells, which leads to the release of inflammatory mediators. The degree of formation of immune complexes depends on the ratio of antibody and antigen in the immune complex. Initially, there is an excess of antigen in small antigen-antibody complexes that do not activate complement. Later, when the number of antibodies and antigens is balanced, immune complexes become larger and tend to be deposited in various tissues (renal glomeruli, blood vessels), which leads to systemic reactions. Type III reactions include serum sickness, SLE (systemic lupus erythematosus), RA (rheumatoid arthritis), leukocytoclastic vasculitis, cryoglobulinemia, hypersensitive pneumonitis, bronchopulmonary aspergillosis, and certain types of glomerulonephritis.

IV type (delayed-type hypersensitivity) are mediated by T lymphocytes. There are 4 subtypes based on the involved subpopulations of T-lymphocytes: T-limimitcii helper type 1 (IVa), T-lymphocytes helper type 2 (IVb), cytotoxic T lymphocytes (IVc), T-lymphocytes secreting IL8 (IVd). These cells, sensitized after contact with a specific antigen, are activated after re-exposure of the antigen; they have a direct toxic effect on the tissues or through released cytokines that activate eosinophils, monocytes and macrophages, neutrophils or killer cells, depending on the type of reaction. Type IV reactions include contact dermatitis (for example, in response to ivy poison), hypersensitivity pneumonitis, allograft rejection reactions, tuberculosis and many forms of drug hypersensitivity.

Intended autoimmune diseases

Probability	Violation	Mechanism or symptom
Highly probable	Autoimmune hemolytic anemia	Phagocytosis of red cell-sensitized antibodies
	Autoimmune thrombocytopenic purpura	Phagocytosis of platelet-sensitized antibodies
	Goodpasture Syndrome	Antibodies to the basal membrane
	Graves disease	Antibodies (stimulating) to the TSH receptor
	Thyroiditis Hashimoto	Cell-based or antibody-mediated thyroid cytotoxicity
	Resistance to insulin	Antibodies to the insulin receptor
	Myasthenia gravis	Antibodies to the acetylcholine receptor
	Pemphigus	Epidermal acantholytic antibodies
	Hard currency	Circulating or locally generalized immune complexes
Probable	Andrenergic drug resistance (in some patients with asthma or cystic fibrosis)	Antibodies to the beta adrenergic receptor
	Bullous pemphigoid	IgG and complement components to the basal membrane
	Diabetes mellitus (some cases)	Cellular or antibody mediated antibodies to islet cells
	Glomerulonephritis	Antibodies or immune complexes to the glomerular basement membrane
	Idiopathic Ad-Dyson Disease	Antibodies or, possibly, cell-associated adrenal cytotoxicity
	Infertility (some cases)	Antisperm antibodies
	Mixed connective tissue diseases	Antibodies to the extracted nuclear antigen (ribonucleoprotein)
	Pernicious anemia	Antibodies to parietal cells, microsomes, internal factor
	Poliomyositis	Non-histone antinuclear antibodies
	RA	Immune complexes in the joints
	Systemic sclerosis with anti-collagen antibodies	Antibodies to the nucleus and nucleolus
	Sjogren's Syndrome	Multiple tissue antibodies, specific non-histone anti-B-B antibodies
Possible	Chronic active hepatitis	Antibodies to smooth muscle cells
	Endocrine gland disorders	Specific tissue antibodies (in some cases)
	Postinfarction, cardiotomy syndrome	Myocardial antibodies
	Primary biliary cirrhosis	Mitochondrial antibodies
	Vasculitis	Lg and complement components in the walls of the vessel, a low level of the serum component (in some cases)
	Vitiligo	Antibodies to melanocytes
	Many other inflammatory, granulomatous, degenerative and atopic disorders	No rational alternative explanation
	Urticaria, atopic dermatitis, asthma (some cases)	IgG and IgM to IgE

TTG - thyrotropic hormone, RA - rheumatoid arthritis, SLE - systemic lupus erythematosus.

[1], [2], [3], [4], [5], [6], [7], [8], [9]