Hypersensitivity, Biology tutorial

Introduction:

The immune system is the integral portion of human protection against disease; however the normally protective immune methods can at times cause detrimental reactions in the host. Such reactions are termed as hypersensitivity reactions, and the study of such is known as immunopathology. The traditional categorization for hypersensitivity reactions is that of Gell and Coombs and is presently the most generally known categorization system. It splits the hypersensitivity reactions into the given four kinds: 

1) Type I reactions (that is, immediate hypersensitivity reactions) comprise immunoglobulin E (IgE) - mediated discharge of histamine and other mediators from the mast cells and basophils. 

2) Type II reactions (that is, cytotoxic hypersensitivity reactions) comprise immunoglobulin G or immunoglobulin M antibodies bound to the cell surface antigens having subsequent complement fixation. 

3) Type III reactions (that is, immune-complex reactions) comprise circulating antigen-antibody immune complexes which deposit in post capillary venules having subsequent complement fixation. 

4) Type IV reactions (that is, delayed hypersensitivity reactions, cell-mediated immunity) are mediated through T cells instead of by antibodies.

Hypersensitivity:

Occasionally, the immune system responds improperly to the presence of antigen. Such responses are termed to as hypersensitivities. There are basically four various kinds of hypersensitivities which outcome from various modifications of the immune system. Such types are categorized as:   

1) Type I: Immediate Hypersensitivity 

2) Type II: Cytotoxic Hypersensitivity 

3) Type III: Immune Complex Hypersensitivity 

4) Type IV: Delayed Hypersensitivity

Type - I Hypersensitivity:

Antigens causing the Type - I hypersensitivity reactions (or immediate-type hypersensitivity) are stated as allergens and persuade the making of antibodies of the IgE isotype in some individuals. IgE-based antibody responses are generally physiologically in parasitic infections however atopic individuals generate IgE responses against the number of non-parasitic antigens which induce either no antibody response or antibody response of various isotype, usually IgG, in normal individuals. Atopic individuals therefore are susceptible to either generalized anaphylaxis or local tissue reactions which comprise a similar pathogenetic method, namely asthma, eczema, hay fever or food allergies.

The tissue response caused due to the type I hypersensitivity reactions is now well understood and is found out by the binding of IgE antibodies to a high affinity receptor that binds the Fc part of IgEs with subnanomolar affinity and is positioned on the membrane of mast cells and basophils. As an outcome, an important fraction of the IgE produced following initial contact having antigen, becomes 'fixed' on the surface of such cells and, in case of a second contact by antigen, the antigen-antibody reactions takes place not just in solution however as well or mostly on the mast cell and basophil membrane.

The IgE-antigen reaction taking place on the surface of basophils and mast cells leads to the receptor cross-linking and degranulation, that is, discharge of vasoactive amines (that is, histamine and serotonin) and other agents (that is, heparin, platelet-activating factor, eosinophil and neutrophil chemotactic factors, a diversity of cytokines and prostaglandins and leukotrienes) from the cytoplasmic granules that collectively cause the contraction of smooth muscle cells, vasodilatation, raised vascular permeability and platelet aggregation and degranulation. Such reactions can influence a single tissue or organ (as in asthma, hay fever and eczema) or multiple ones (that is, as in generalized anaphilaxis) based on local or general re-exposure to the allergen.

Type - II Hypersensitivity:

Dissimilar to Type - I reactions, Type - II hypersensitivity is mainly caused due to direct antibody-mediated cell damage or lysis. The real methods underlying cell destruction are multiple:

1) Complement-dependent red blood cell lysis, for illustration as an outcome of haemolytic transfusion reactions (HTR) caused due to ABO incompatibility and in the other forms of haemolytic anemia.

2) Antibody-dependent red blood cell degradation takes place, for illustration as the outcome of binding of antibodies to the red cell membrane that fail to activate complement however promote macrophage uptake and RBC degradation. This takes place for illustration in the haemolytic disease of the newborn (HDN) caused due to Rh incompatibility.

3) Antibody-dependent cell-mediated cytotoxicity (ADCC) that takes place if cytotoxic antibodies become fixed on the surface of cytotoxic T cells and ensuing antigen binding induce perforin-dependent cell lysis of the cell bearing the antigen.

Type - III Hypersensitivity:

Type - III hypersensitivity reactions are mainly caused due to antibody-antigen complexes. If significant quantities of these immune complexes are made, they can deposit in tissues and lead to the tissue reaction that is initiated through complement activation and leads to the mast cell leukocyte, degranulation, predominantly neutrophil, chemotaxis and an inflammatory reactions caused due to the activation of such cells.

There are systemic varieties of type III hypersensitivity reactions, like serum sickness, a disease that is now of pure historic interest however was a general occurrence in patients receiving the repeated injections of anti-diphteric horse serum and in which the immune complex deposition occurred in a diversity of tissues and organs leading to fever, generalized vacuities having edema and erhytema, glomerulonephritis and arthritis.

There are as well local forms of immune complex diseases, like the Arthus phenomenon. In the systemic and local forms of type III hypersensitivity reactions, the emergence and also the resolution of the tissue lesions and clinical signs follows firmly the construction of the immune complexes, the cause damage of tissue. The main method responsible for tissue damage as an outcome of deposition of immune complexes is mediated through complement components, mostly the C3a and C5a anaphylotoxins which fascinate phagocytes and mast cells and, following binding to complement receptors on the surface of these cells, lead to the degranulation causing the local inflammatory reaction (that is, vasodilatation, raised vascular permeability and so on).

Type - IV Hypersensitivity

The prototypical type - IV (or delayed-type hypersensitivity, DTH) tissue reaction is basically the phenomenon introduced by Koch. Type -IV hypersensitivity reactions are mainly caused due to activated TH1 cells which are activated through intracellular pathogens, comprising bacteria, protozoa and fungi and also some chemicals (such as hair dyes and nickel salts) leading to the clonal expansion and differentiation of antigen-specific cells into TH1 clones. This corresponds to the sensitization stage of DTH.

On re-encounter by the antigen, in the so-called effectors stage, the antigen-specific TH1 clones experience further clonal expansion and secretion of a diversity of effectors molecules. Such comprise both cytokines (like IFN-gamma, TNF-beta, IL-2 and IL-3) and chemokines like IL-8, monocyte chemotactic and activating factor (MCAF) and a migration inhibiting factor (or MIF) which together lead to the macrophage activation and to the growth of a local tissue reaction.

Therefore DTH is eventually mediated through the macrophages recruited and activated through the products of antigen-specific TH1 clones. Dissimilar to type I, II and III reactions which can be transferred by means of serum (that is, serum antibodies), passive transfer of type IV needs the transfer of antigen-specific TH1 clones which orchestrate the macrophage response.

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