Here is an essay on ‘Hypersensitivity Reactions’ for class 8, 9, 10, 11 and 12. Find paragraphs, long and short essays on ‘Hypersensitivity Reactions’ especially written for school and medical students.
Essay on Hypersensitivity Reactions
Immune reactions indicate a means of protection against infection due to development of specific resistance. Certain immunological reactions produce tissue damage during antigen and antibody reaction, instead of protection, by direct action or due to release of pharmacologically active substances. These are known as hypersensitivity reactions.
Broadly, there are two forms of hypersensitivity reactions:
1. Reactions Mediated by Humoral Antibodies (Immediate Type):
i. Type I Reaction
ii. Type II Reaction
iii. Type III Reaction.
2. Reaction Mediated by Cell-Mediated Immune Response:
Type IV Reaction (Delayed type of hypersensitivity).
Essay # 1. Reactions Mediated by Humoral Antibodies:
i. Type I Reaction: Anaphylactic Reaction:
In man there are two types of anaphylactic reactions. These depend upon the portal of entry of the antigen, (a) The systemic reactions occur when the antigen is infected parenterally as in the case of foreign sera, drugs—like penicillin or even bites of insects or during desensitisation with pollen extracts. This is manifested by bronchospasm, laryngeal oedema, dyspnoea, cyanosis and fall of blood pressure. Cutaneous wheal or urticaria occurs during absorption through intestinal mucosa. There may be diarrhoea and nausea, (b) The local reactions are due to pollen, dander, house dust, animal food, etc. These act on the respiratory mucosa causing asthma or hay fever, on the conjunctiva causing conjunctivitis, and on the nasal mucosa causing rhinorrhea.
The IgE class antibody involved in this reaction has strong affinity for tissue of the same species, (homocytotrophic). After sensitisation when an individual again comes into contact with antigen, anaphylactic reaction sets off. In this reaction there is not sufficient IgE antibody in circulation to mop up the antigen.
Initial binding of IgE to the Fc fragment of mast cell and its subsequent interaction with antigen on the cell membrane of the mast cell with entry of calcium releases pharmacological mediators, e.g., histamine, slow reacting substance of anaphylaxis (SRS-A), serotonin, plasma kinin, prostaglandins and eosinophil chemotactic factor of anaphylaxis (ECF-A) and platelet activating factor (PAF). Recent works indicate that two adjacent IgE molecules must be bridged by an antigen before degranulation of mast cell can occur. Monovalent antigen will only block the antibody IgE and will not set off the reaction.
Histamine from its precursor histidine in the granules of mast cells causes vasodilation. It also liberates 5-HT or serotonin which causes contraction of smooth muscles and increases capillary permeability. SRS-A has contracting effect on smooth muscles of blood vessels. Plasma kinin liberates bradykinin, acts like histamine and also like an enzyme aryl sulphatase, which inactivates SRS-A. ECF-A is related to repair of tissue damage in this reaction.
ii. Type II Reaction: Cytotoxic For Cytolytic Reaction:
This is initiated by an antigenic component which is a part of or a small molecule attached to the cell surface. The antibodies either IgG or IgM class are directed against their antigens bringing about cytotoxic or cytolytic effect involving complement. These are observed in haemolytic disease of the new-born, sedormid purpura and certain bacterial infections.
Haemolytic disease of the new-born is caused by Rhesus incompatibility between mother and foetus, when a Rh (-ve) mother carries Rh (+vc) foetus in the first pregnancy, the latter having inherited Rh antigen from its Rh (+ve) father. If the foetal red cells enter maternal circulation in sufficient quantity at the time of delivery, anti-Rh (+ve) (IgM and IgG) antibodies arc found 6-8 weeks after delivery, but not during the course of the first pregnancy although the foetal red cells are introduced into the mother’s circulation throughout pregnancy but not in sufficient amount to elicit immunological response.
In the subsequent pregnancy the only circulating anti-Rh IgG antibodies from the maternal circulation pass across the placental circulation and react with Rh antigen of foetal red cells. These antibody coated cells are then phagocytosed and destroyed by the macrophages in the foetal liver and spleen.
This results in haemolytic anaemia. In such cases if there be ABO incompatibility between the mother and foetus along with Rh incompatibility, the small number of foetal cells that cross the placenta are rapidly haemolysed by maternal antibodies against the foetal red cells. So Rh sensitisation will not occur. Thus, ABO incompatibility in the first and subsequent pregnancies will protect mother from Rh immunisation until she carries ABO compatible foetus.
iii. Type III Reaction: Tissue Damage by Immune Complexes:
This reaction falls into two categories:
(a) Local reaction—Arthus phenomenon.
(b) Systemic reaction – Serum sickness.
(a) Local Reaction:
Arthus phenomenon is a local reaction at the site of entry of antigen. This occurs in the wall of small blood vessels in the presence of large amount of IgG antibody forming micro precipitate both intravascular and extravascular tissue with activation of complement.
This results in inflammation with liberation of vaso-active amines causing vasodilatation and chemotaxis for neutrophils. This is seen at the site of injection of insulin in diabetes or in asthmatic reaction in allergic alveolitis following inhalation of mouldy hay, after frequent immunisation with toxoids and following intradermal injection of fungal antigen in cases of Farmer’s lungs.
(b) Systemic Reaction:
Serum sickness was initially described in individuals treated with anti- diphtheritic horse serum foreign to the host. The individual may develop anaphylactoid reaction within a few minutes, if there be previous contact with antigen and residual antibody be present in circulation.
The anaphylactoid reactions are due to IgE antibodies attached to the mast cells and subsequent setting off a chain of events, but the tissue damage is caused by combination of excess of antibody with soluble antigen forming complexes deposited on the blood vessels, where they activate the complement leading to inflammation and chemotaxis or neutrophils.
The intensity of reaction depends upon the concentration of complexes and on the type of the antibody on activating the complement since IgM, IgG, IgG2 and IgG3 can activate complement but not other antibodies (IgG4 and IgA dimer). Apart from typical serum sickness, in a number of infectious diseases the development of tissue damage occurs in this mechanism and could be featured as a failure in cell-mediated immunity, but not in humoral immunity. Certain organisms like mycobacteria or viruses need cell-mediated immunity for their eradication.
The infecting organism proliferates as a result of specific failure of T-cell function and soluble bacterial or viral antigen is released into the circulation. The latter will stimulate B-cell to produce large amount of humoral antibodies because of lack of ‘suppressor’ to T-cell. The latter will react with antigen and form immune-complexes in the wall of blood vessels.
Antigens derived from infective micro-organism have been demonstrated in the immune-complexes in the glomeruli in malarial infection in children, in the skin as cutaneous vasculitis in lepromatous leprosy (erythema nodosum leprosum), in kidney deposits of certain surface antigen of hepatitis B virus.
Immune- complex glomerulonephritis occurs as a part of infection by virus, bacteria and parasite, autoimmune disorder and immune-reaction to drugs like penicillin, streptomycin and sulphonamide. Arthritis as manifestation of an immune-complex disease is associated with drug for hypertension, SLE, following recovery from meningococcal infection and viral disease such as rubella.
Essay # 2. Type IV Reaction: Reaction Caused by Cell-Mediated Immune Responses:
Initial antigenic stimulus produces virgin T-cells to sensitised T-lymphocytes. These cells are always passing through the tissue since 70%-80% of circulating lymphocytes are T-cells. These sensitised T-cells may have some receptor-like from their cell wall or may be a substance secreted by the cell on its surface in a soluble form. On subsequent challenge a single sensitised lymphocyte at the site of antigen deposition sets up reactions bringing in a small number of sensitized lymphocytes which also act with antigen. They release pharmacologically soluble mediator, lymphokines.
The latter first act directly as being chemotactic for macrophages and then act directly by causing a decreased electrostatic charge on the surface of these cells as a result of which they tend to aggregate in the lesion. The non-sensitized lymphoid cells from the bone marrow are also drawn into the site of reaction directly. These cells are related enzymatically to the macrophages.
The latter activate complement through their Fc receptor and receptor for CI, and initiate inflammation. This is the mechanism of delayed hypersensitivity in man. This can be demonstrated against bacteria, e.g., myco. tuberculosis, myco. leprae, brucella; viruses, e.g., vaccinia, paramyxovirus, herpes; fungi, e.g., candidiasis, histoplasmosis, coccidiomycosis; and protozoa, e.g., leishmania. Similar phenomenon is also observed in allograft (homograft) reaction. This reaction is also observed with chemicals, like dinitrochlorobenzene, picryl chloride, and phenyl hydrazine, following contact with skin and following contact of metals, e.g., mercury, nickel, chromium with skin.
Certain insect bites like mosquitoes produce red induration which is due to delayed hypersensitivity and is directed to an antigen present in the saliva of mosquitoes. Reactions to stings from bees, wasps and hornets are usually anaphylactic.