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Drugs & Diseases > Allergy & Immunology

Immediate Hypersensitivity Reactions

Updated: Feb 09, 2015
Author: Becky Buelow, MD, MS; Chief Editor: Michael A Kaliner, MD more...

Background
The immune system is an integral part of human protection against disease, but the
normally protective immune mechanisms can sometimes cause detrimental
reactions in the host. Such reactions are known as hypersensitivity reactions, and
the study of these is termed immunopathology. The traditional classification for
hypersensitivity reactions is that of Gell and Coombs and is currently the most
commonly known classification system. [1] It divides the hypersensitivity reactions
into the following 4 types:
Type I reactions (ie, immediate hypersensitivity reactions) involve
immunoglobulin E (IgE)mediated release of histamine and other mediators
from mast cells and basophils. [2] Examples include anaphylaxis and allergic
rhinoconjunctivitis.
Type II reactions (ie, cytotoxic hypersensitivity reactions) involve
immunoglobulin G or immunoglobulin M antibodies bound to cell surface
antigens, with subsequent complement fixation. An example is drug-induced
hemolytic anemia.
Type III reactions (ie, immune-complex reactions) involve circulating
antigen-antibody immune complexes that deposit in postcapillary venules,
with subsequent complement fixation. An example is serum sickness.
Type IV reactions (ie, delayed hypersensitivity reactions, cell-mediated
immunity) are mediated by T cells rather than by antibodies. An example is
contact dermatitis from poison ivy or nickel allergy.
Some authors believe this classification system may be too general and favor a
more recent classification system proposed by Sell et al. [3] This system divides
immunopathologic responses into the following 7 categories:
Inactivation/activation antibody reactions
Cytotoxic or cytolytic antibody reactions
Immune-complex reactions
 Allergic reactions
T-cell cytotoxic reactions
Delayed hypersensitivity reactions
Granulomatous reactions
This system accounts for the fact that multiple components of the immune system
can be involved in various types of hypersensitivity reactions. For example, T cells
play an important role in the pathophysiology of allergic reactions (see
Pathophysiology). In addition, the term immediate hypersensitivity is somewhat of
a misnomer because it does not account for the late-phase reaction or for the
chronic allergic inflammation that often occurs with these types of reactions.
Allergic reactions manifest clinically as anaphylaxis, allergic asthma, urticaria,
angioedema, allergic rhinitis, some types of drug reactions, and atopic dermatitis.
These reactions tend to be mediated by IgE, which differentiates them from non-
IgE-mediated (formerly called anaphylactoid) reactions that involve IgE-
independent mast cell and basophil degranulation. Such reactions can be caused by
iodinated radiocontrast dye, opiates, or vancomycin and appear similar clinically to
urticaria or even anaphylaxis. [4, 5]
Patients prone to IgE-mediated allergic reactions are said to be atopic. Atopy is the
genetic predisposition to make IgE antibodies in response to allergen exposure. [6]
The focus of this article is allergic reactions in general. Although some of the
clinical manifestations listed previously are briefly mentioned, refer to the articles
on these topics for more detail. For example, see Allergic and Environmental
Asthma;Anaphylaxis; Food Allergies; Rhinitis, Allergic; and Urticaria.
Next: Pathophysiology

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