Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. They are usually referred to as an over-reaction of the immune system and these reactions may be damaging and uncomfortable. This is an immunologic term and is not to be confused with the psychiatric term of being hypersensitive which implies to an individual who may be overly sensitive to physical (i.e. sound, touch, light, etc.) and/or emotional stimuli. Although there is a relation between the two – studies have shown that those individuals that have ADHD (a psychiatric disorder) are more likely to have hypersensitivity reactions such as allergies, asthma, eczema than those who do not have ADHD. Hypersensitivity reactions can be classified into four types.

Type I: IgE mediated immediate reaction

Type II: Antibody-mediated reaction (IgG or IgM antibodies)

Type III: Immune complex-mediated reaction

Type IV: Cytotoxic, cell-mediated, delayed hypersensitivity reaction

The first three types are considered immediate hypersensitivity reactions because they occur within 24 hours. The fourth type is considered a delayed hypersensitivity reaction because it usually occurs more than 12 hours after exposure to the allergen, with a maximal reaction time between 48 and 72 hours.

Type I hypersensitivity occurs as a result of exposure to an antigen. The response to the antigen occurs in two stages: the sensitization and the effect stage. In the "sensitization" stage, the host experiences an asymptomatic contact with the antigen. Subsequently, in the "effect" period, the pre-sensitized host is re-introduced to the antigen, which then leads to a type I anaphylactic or atopic immune response. Type II hypersensitivity reaction refers to an antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens with the resultant cellular destruction, functional loss, or damage to tissues.

Type II hypersensitivity

Damage can be accomplished via three different mechanisms:

• Antibody binding to cell surface receptors and altering its activity
• Activation of the complement pathway.
• Antibody-dependent cellular cytotoxicity.

The pathophysiology of type II hypersensitivity reactions can be broadly classified into three types:

• Cell depletion or destruction without inflammation
• Inflammation mediated by complement or Fc receptor
• Cellular dysfunction by antibodies

The process involves a series of immune-mediated events that might take different forms.

In type III hypersensitivity reaction, an abnormal immune response is mediated by the formation of antigen-antibody aggregates called "immune complexes". They can precipitate in various tissues such as skin, joints, vessels, or glomeruli, and trigger the classical complement pathway. Complement activation leads to the recruitment of inflammatory cells (monocytes and neutrophils) that release lysosomal enzymes and free radicals at the site of immune complexes, causing tissue damage. The most common diseases involving a type III hypersensitivity reaction are serum sickness, post-streptococcal glomerulonephritis, systemic lupus erythematosus, farmers' lung (hypersensitivity pneumonitis), and rheumatoid arthritis. The principal feature that separates type III reactions from other hypersensitivity reactions is that in type III reaction, the antigen-antibody complexes are pre-formed in the circulation before their deposition in tissues.

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Journal of Clinical Immunology and Allergy