hypersensitivity Flashcards
(5 cards)
What are the major types of hypersensitivity reactions?
Immediate hypersensitivity (type I hypersensitivity) is caused by the release of mediators from mast cells triggered by antigen cross-linking of IgE bound to IgE
receptors. Antibodies specific for cell or tissue antigens can cause damage by activating
complement and engaging phagocytes (type II hypersensitivity); antibodies can also destroy circulating cells and block the functions of essential molecules or their receptors. Antibody-antigen complexes (immune complexes) deposit in blood vessels, causing
inflammation and thrombosis, leading to tissue injury (type III hypersensitivity). Reactions of T lymphocytes can cause inflammation and tissue damage (type IV hypersensitivity, cell-mediated, delayed-type hypersensitivity).
What is the sequence of events in a typical immediate hypersensitivity reaction? What
is the late-phase reaction, and how is it caused?
Exposure to an environmental antigen induces differentiation of IL-4 producing helper
T cells, which in turn induce IgE antibody responses to the same antigen. The IgE binds
to high-affinity IgE receptors on mast cells in tissues throughout the body. On
subsequent exposure to the same antigen, the mast cell–bound IgE molecules bind the
antigen and become cross-linked, generating signals from the associated Fcε receptors
that lead to mast cell granule release (degranulation), enzymatic generation of
leukotrienes and prostaglandins, and synthesis of cytokines. Vasoactive amines such as
histamine, released from the granules, and prostaglandins cause acute vascular changes
leading to increased blood vessel permeability and edema, usually within minutes of
exposure to the antigen. The late-phase reaction is an inflammatory response in which
blood leukocytes are recruited to the site of mast cell degranulation, caused by TNF and
other cytokines secreted by the mast cells.
What are some examples of immediate hypersensitivity disorders, what is their
pathogenesis, and what are the principles for treatment?
Allergic rhinitis is one type of immediate hypersensitivity reaction to inhaled allergens,
such as pollen proteins, leading to upper airway mucosal mast cell secretion of
histamine and long-lasting inflammation due to various cytokines. Allergic bronchial
asthma is caused by inhaled allergens inducing bronchial mast cell release of mediators,
including leukotrienes, which cause bronchial constriction and airway obstruction,
excessive secretion of mucus in the airways, and bronchial smooth muscle hypertrophy.
Anaphylaxis is a severe systemic immediate hypersensitivity reaction characterized by
shock and airway obstruction resulting from mast cell degranulation in many tissue
sites, usually after exposure to an antigen that is injected or ingested.
Immediate hypersensitivity disorders are treated by inhibiting mast cell activation,
mediator actions, Th2 responses and late-phase inflammation.
How do antibodies (IgG and IgM) and immune complexes cause tissue injury and
disease? What are the examples of diseases they cause?
Antibodies cause tissue injury and disease by activating cytotoxic and inflammatory
effector functions, mainly complement activation and opsonization and phagocytosis
via Fc receptors. Some antibodies may cause disease by binding to and interfering with
the normal function of a particular protein. Diseases: haemolytic disease of the newborn, Graves disease, Myasthenia gravis.
Immune complexes deposit in the walls of blood vessels and cause inflammation of the
vessel (vasculitis), which leads to blood clotting in the vessel lumen (thrombosis) and
loss of blood supply to tissues supplied by the vessels. The site of immune complex
deposition is not related to the specificity of the antibodies. Therefore, immune complex
disease may simultaneously affect many different tissue sites. Diseases: Arthus reaction,
Serum sickness.
. What are some examples of hypersensitivity reactions caused by T cells, what is their
pathogenesis?
Contact hypersensitivity (e.g., poison ivy, nickel hypersensitivity) is caused by T cells
specific for skin proteins that are modified by plant toxins, metals, and other chemicals,
leading to inflammation and blistering. Tuberculin skin test reaction is caused by
antigen-specific Th1 cells which induce recruitment of phagocytes to the site of
injection to cause visible lesions.
