Hypersensitivity is defined as an abnormal, exaggerated immune reaction to a foreign agent, with resulting injury to host tissues. Four different mechanisms of hypersensitivity have been elucidated (Table 8-1). All forms except type IV are mediated by humoral mechanisms (ie, by antibodies); type IV hypersensitivity is cell-mediated. In all forms, initial exposure (sensitizing dose) to the antigen involved evokes a primary immune response (sensitization). Following a short period (1 or more weeks) during which the immune system is activated, a hypersensitivity response occurs upon any subsequent exposure (challenge dose) to that antigen.
Type I (Immediate) Hypersensitivity (Atopy; Anaphylaxis)
(Figure 8-1.) The first exposure to an antigen (allergen) activates the immune system and causes production of IgE antibodies (reagins) specifically reactive against the antigen. These become attached to the surface membrane of mast cells and basophils through high-affinity IgE Fc receptors. Production of sufficient antibody to develop clinical hypersensitivity takes 1 or more weeks. When subsequent exposure to the same antigen occurs, an antigen-antibody (IgE) interaction takes place on the surface of the mast cell or basophil and causes degranulation of these cells. The cytoplasmic granules of mast cells release vasoactive substances (histamine and a variety of enzymes that generate bradykinin and leukotrienes [Chapter 3: The Acute Inflammatory Response]) that cause vasodilation, increased vascular permeability, and smooth muscle contraction. Mast cells also release factors that are chemotactic for neutrophils and eosinophils; many lesions caused by type I hypersensitivity contain numerous eosinophils in affected tissues and peripheral blood. Eosinophils activate both the coagulation and complement systems and promote further degranulation of basophils and mast cells. However, eosinophils also release arylsulfatase B and histaminase, which serve to cleave leukotrienes and histamine, respectively, thereby down-modulating the allergic response.
Type I hypersensitivity. The first (sensitizing) dose of antigen results in production of specifically reactive IgE that becomes adsorbed on the surface of mast cells. A second exposure to the antigen results in an antigen-antibody reaction on the mast cell surface, causing rapid release by the mast cell of vasoactive substances responsible ...
Log In to View More
If you don't have a subscription, please view our individual subscription options below to find out how you can gain access to this content.
Want remote access to your institution's subscription?
Sign in to your MyAccess profile while you are actively authenticated on this site via your institution (you will be able to verify this by looking at the top right corner of the screen - if you see your institution's name, you are authenticated). Once logged in to your MyAccess profile, you will be able to access your institution's subscription for 90 days from any location. You must be logged in while authenticated at least once every 90 days to maintain this remote access.
If your institution subscribes to this resource, and you don't have a MyAccess profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus.
AccessPhysiotherapy Full Site: One-Year Subscription
Connect to the full suite of AccessPhysiotherapy content and resources including interactive NPTE review, more than 500 videos, Anatomy & Physiology Revealed, 20+ leading textbooks, and more.
Pay Per View: Timed Access to all of AccessPhysiotherapy
24 Hour Subscription $34.95
48 Hour Subscription $54.95
Pop-up div Successfully Displayed
This div only appears when the trigger link is hovered over.
Otherwise it is hidden from view.