Hypersensitivity Reaction Paper
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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.Hypersensitivity Reaction Paper
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. Hypersensitivity Reaction Paper 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.Hypersensitivity Reaction Paper
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.Hypersensitivity Reaction Paper
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.Hypersensitivity Reaction Paper
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.Hypersensitivity Reaction Paper
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