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Hypersensitivity - An Overview
This Sqadia lecture elucidate how the disease are caused by immune responses. Hypersensitivity refers to excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. Hypersensitivity reactions can be divided into four types: type I, type II, type III and type IV, based on the mechanisms involved and time taken for the reaction. Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced haemolytic anaemia, granulocytopenia and thrombocytopenia are such examples.
Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms. They usually form when antigen is produced in excess of antibody. Immune complexes may arise from antigen formed from infectious agents, innocuous environmental antigen or autoantigen cross reacting with autoantibody. They may be localised to the site of antigen production or they may be found in the circulation. Immune complexes are usually cleared by the classical complement pathway or by the transfer of immune complexes by red blood cells to the liver or spleen for phagocytosis. The clearing mechanisms may be inadequate when there is excessive production of immune complexes.
Role of Complement System in Hypersensitivity
Complement is actually composed of over 20 different serum proteins that are produced by a variety of cells including, hepatocytes, macrophages and gut epithelial cells. Contribute to host defenses. Complement can opsonize bacteria for enhanced phagocytosis; it can recruit and activate various cells including PMNs and macrophages. It can participate in regulation of antibody responses and it can aid in the clearance of immune complexes and apoptotic cells. Complement can also have detrimental effects for the host; it contributes to inflammation and tissue damage and it can trigger anaphylaxis. Complement has a central role in inflammation as it causes chemotaxis of phagocytes, opsonization and lysis of pathogens and clearance of immune complexes. Chelating agents dismantle the C1 complex and are anti-complementary.
Type IV hypersensitivity is often called delayed type hypersensitivity. The reaction takes two to three days to develop. This is the only class of hypersensitive reactions to be triggered by antigen-specific T cells. TH1 cells but they were originally termed TDTH after the alternative name for this reaction delayed type hypersensitivity. It is usually maximal in 48-72 hours. Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the bulk of the damage. The delayed hypersensitivity lesions mainly contain monocytes and a few T cells. Development of delayed-type hypersensitivity reaction after a second exposure to poison oak. Tissue damage results from lytic enzymes released from activated macrophages. DTH is not always detrimental. Granuloma formation (fusion of continuously activated macrophages leads to giant multinucleated cells). These giant cells displace the normal tissue cells, forming palpable nodules.
Contribution of Environmental Factors in Allergy
Environmental factors and genetic variation each account for about 50%. The prevalence of atopic allergic diseases is increasing in economically advanced regions. Environmental changes involve exposure to infectious diseases in early childhood. Change from traditional rural society meant less exposure to microbes. Changes in intestinal microbiota idea that exposure to microorganisms is associated with allergy was first mooted in 1989 hygiene hypothesis. Probiotics can be a safe and effective approach to preventing various allergic diseases by modifying the gut microbiota, but further work is needed to determine the exact mechanism and the most optimal composition.