This document discusses hypersensitivity and immune-mediated disorders. It defines hypersensitivity as an immunologic reaction that causes tissue damage upon reexposure to an antigen. There are four types of hypersensitivity reactions classified by Gell and Coombs: type I involves IgE antibodies, type II involves IgG antibodies and complement, type III involves immune complex formation, and type IV involves delayed-type hypersensitivity and T cells. Causes of hypersensitivity diseases include reactions against self-antigens due to failures in self-tolerance (autoimmunity), reactions against microbes, and reactions against environmental antigens. Diseases can be caused by antibodies against cells/tissues or immune complexes deposited in tissues.
A. There are three types of immunological disorders
1. Hypersensitivity
2. Autoimmune disease
3. Immunodeficiency
B. Hypersensitivity reactions to usually harmless substances are often called allergies or allergic reactions
Concepts of hypersensivity should be well versed to all medical personnel to understand its implications. I have made it very simple to all readers to understand the same
A. There are three types of immunological disorders
1. Hypersensitivity
2. Autoimmune disease
3. Immunodeficiency
B. Hypersensitivity reactions to usually harmless substances are often called allergies or allergic reactions
Concepts of hypersensivity should be well versed to all medical personnel to understand its implications. I have made it very simple to all readers to understand the same
Through this presentation you will be able to learn detailed information about hypersensitivity reactions, its type and clinical manifestation of all types of hypersensitivity reactions and related diseases.
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is 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.
Immunofluorescence : Immunofluorescence is a powerful technique that utilizes fluorescent-labeled antibodies to detect specific target antigens..
Fluorescein is a dye which emits greenish fluorescence under UV light. It can be tagged to immunoglobulin molecules.
This technique is sometimes used to make viral plaques more readily visible to the human eye.
Immunofluorescent labeled tissue sections are studied using a fluorescence microscope.
Normally the immune system plays an important role in protecting the body from microorganisms and other foreign substances. If the activity of the immune system is excessive or overreactive, a hypersensitivity reaction develops. The consequences of a hypersensitivity reaction may be injury to the body or death.
Through this presentation you will be able to learn detailed information about hypersensitivity reactions, its type and clinical manifestation of all types of hypersensitivity reactions and related diseases.
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is 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.
Immunofluorescence : Immunofluorescence is a powerful technique that utilizes fluorescent-labeled antibodies to detect specific target antigens..
Fluorescein is a dye which emits greenish fluorescence under UV light. It can be tagged to immunoglobulin molecules.
This technique is sometimes used to make viral plaques more readily visible to the human eye.
Immunofluorescent labeled tissue sections are studied using a fluorescence microscope.
Normally the immune system plays an important role in protecting the body from microorganisms and other foreign substances. If the activity of the immune system is excessive or overreactive, a hypersensitivity reaction develops. The consequences of a hypersensitivity reaction may be injury to the body or death.
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Normally, immune responses eradicate infectious pathogens without serious injury to host tissues.
However, these responses are sometimes
inadequately controlled
inappropriately targeted to host tissues
triggered by commensal microorganisms or environmental antigens that are usually harmless.
In these situations, the normally beneficial immune response is the cause of disease.
Disorders caused by immune responses are called hypersensitivity diseases.
This term , hypersensitivity , arose from the clinical definition of immunity as sensitivity, which is based on the observation that an individual who has been exposed to an antigen exhibits a detectable reaction, or is sensitive, to subsequent encounters with that antigen.
Today, we will describe the pathogenesis of different types of hypersensitivity reactions, with an emphasis on the effector mechanisms that cause tissue injury.
A variety of human diseases are caused by immune responses to non-microbial environmental antigens, and involve the type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13 produced by Th2 cells and innate lymphoid cells (ILCs), immunoglobulin E (IgE), mast cells, and eosinophils.
The antigens that elicit immediate hypersensitivity are called allergens. Most of them are common environmental proteins, animal products, and chemicals that can modify self proteins.
In the effector phase of these responses, mast cells and eosinophils are activated to rapidly release mediators that cause
increased vascular permeability
Vasodilation
bronchial and visceral smooth muscle contraction
This vascular reaction is called immediate hypersensitivity because it begins rapidly, within minutes of antigen challenge in a previously sensitized individual (immediate), and has major pathologic consequences (hypersensitivity).
Following the immediate response, there is a more slowly developing inflammatory component called the late-phase reaction characterized by the accumulation of neutrophils, eosinophils, and macrophages.
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1. Type I Hypersensitivity:
Type I hypersensitive reactions are the commonest type among all types which is mainly induced by certain type of antigens i.e. allergens. Actually anaphylaxis means “opposite of protection” and is mediated by IgE antibodies through interaction with an allergen
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2. Gell and Coombs Classification
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•
•
•
Type I (IgE-mediated)
Type II (Fc and complement-mediated)
Type III (Immune complex-mediated)
Type IV (Delayed-type hypersensitivity)
4. CAUSES OF HYPERSENSITIVITY DISEASES
• Autoimmunity.
• Failure of the normal mechanisms of self-tolerance results
in reactions against one’s own cells and tissues.
• Autoimmune diseases are estimated to affect 2% to 5% of
the population in developed countries.
• The incidence of these disorders is rising. Many of these
diseases are common in individuals 20- to 40y .
• They are more common in women than in men.
• Autoimmune diseases are chronic and debilitating.
• Many new treatments for these disorders have been
developed based on scientific principles.
5. •
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•
•
•
•
•
•
•
•
Reactions against microbes.
Immune responses against microbial antigens may cause disease if the reactions are
excessive or the microbes are unusually persistent.
T cell responses against persistent microbes may give rise to severe inflammation,
sometimes with the formation of granulomas; this is the cause of tissue injury in
tuberculosis and some other chronic infections.
If antibodies are produced against microbial antigens, the antibodies may bind to
the antigens to produce immune complexes, which deposit in tissues and trigger
inflammation.
Rarely, antibodies or T cells against a microbe may cross-react with a host tissue.
In some diseases involving the intestinal tract, called inflammatory bowel disease,
the immune response is directed against commensal bacteria that normally reside in
the gut and cause no harm.
Sometimes the disease-causing immune response may be entirely normal, but in the
process of eradicating the infection, host tissues are injured.
In viral hepatitis, the virus that infects liver cells is not cytopathic, but it is
recognized as foreign by the immune system.
Cytotoxic T lymphocytes (CTLs) try to eliminate infected cells, and this normal
immune response damages liver cells.
This type of normal reaction is not considered hypersensitivity.
6. • Reactions against environmental antigens.
• Most healthy individuals do not react against
common, generally harmless environmental
substances.
• 20% of the population is abnormally responsive to
one or more of these substances.
• These individuals produce immunoglobulin E
(IgE) antibodies that cause allergic diseases.
• Some individuals become sensitized to
environmental antigens and chemicals that contact
the skin and develop T cell reactions that lead to
cytokine-mediated inflammation, resulting in
contact sensitivity.
7. DISEASES CAUSED BY ANTIBODIES
• Antibody-mediated diseases are produced either by antibodies
that bind to antigens on particular cells or in extracellular
tissues or by antigen-antibody complexes that form in the
circulation and are deposited in vessel walls.
• The lesions can be induced in a normal animal by the
adoptive transfer of immunoglobulin purified from the blood
or affected tissues of individuals with the disease.
• It is occasionally seen in children of mothers suffering from
antibody-mediated diseases.
• These infants may be born with transient
manifestations because of transplacental passage of
antibodies.
8. Diseases Caused by Antibodies Against Fixed
Cell and Tissue Antigens
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•
•
•
Antibodies against tissue antigens cause disease by three main
mechanisms:
1) Antibodies that bind to cell surface antigens
- may directly opsonize cells
- may activate the complement system
resulting in the production of complement proteins that opsonize cells.
These opsonized cells are phagocytosed and destroyed by phagocytes
that express receptors for the Fc portions of IgG antibodies and
receptors for complement proteins.
This is the principal mechanism of cell destruction in
1- Autoimmune hemolytic anemia.
2- Autoimmune thrombocytopenic purpura.
3- Hemolysis in transfusion reactions.
9. • 2) Antibodies deposited in tissues recruit
neutrophils and macrophages, which bind to the
antibodies or to attached complement proteins by
IgG Fc and complement receptors.
• These leukocytes are activated by signaling from
Fc receptors, and leukocyte products, including
lysosomal enzymes and reactive oxygen species,
are secreted and cause tissue injury.
• The mechanism of injury in antibody mediated
glomerulonephritis and many other diseases is
inflammation and leukocyte activation.
10. • 3) Antibodies that bind to normal cellular
receptors or other proteins may interfere
with the functions of these receptors or
proteins and cause disease without
inflammation or tissue damage.
• Antibody-mediated functional abnormalities
are the cause of Graves’ disease and
myasthenia gravis.
gravis
11.
12. Immune Complex–Mediated Diseases
• Immune complexes that cause disease composed of
antibodies bound to either self antigens or foreign
antigens.
• The pathologic features of diseases caused by
immune complexes reflect the site of immune
complex deposition.
• Not determined by the cellular source of the
antigen.
• Therefore, immune complex–mediated diseases
tend to affect multiple tissues and organs.
13. •
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•
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The occurrence of diseases caused by immune complexes was
suspected.
At that time, diphtheria infections were being treated with serum from
horses immunized with the diphtheria toxin.
von Pirquet noted that joint inflammation (arthritis), rash, and fever
developed in patients injected with the antitoxin-containing horse
serum.
It was not due to the infection or a toxic component of the serum itself.
First, these symptoms appeared even after the injection of horse serum
not containing the antitoxin, so it is not due to the anti-diphtheria
antibody.
Second, the symptoms appeared at least a week after the first injection
of horse serum and more rapidly with each repeated injection.
So this disease was due to a host response to some component of the
serum.
The host made antibodies to horse serum proteins, these antibodies
formed complexes with the injected proteins, and the disease was due
to the antibodies or immune complexes.
He called this serum sickness and it is the prototype for systemic
immune complex–mediated disorders.
14.
15.
16.
17.
18. Diseases Caused by Antibodies Against Fixed
Cell and Tissue Antigens
• 1)Antibodies that bind to cell surface antigens may directly
opsonize cells, or they may activate the complement
system, resulting in the production of complement proteins
that opsonize cells.
• These opsonized cells are phagocytosed and destroyed by
phagocytes that express receptors for the Fc portions of
IgG antibodies and receptors for complement proteins.
• This is the principal mechanism of cell destruction in
autoimmune hemolytic anemia and autoimmune
thrombocytopenic purpura.
• The same mechanism is responsible for hemolysis in
transfusion reactions
19. • 2)Antibodies deposited in tissues recruit neutrophils and
macrophages, which bind to the antibodies or to attached
complement proteins by IgG Fc and complement receptors.
• These leukocytes are activated by signaling from the
receptors, particularly Fc receptors, and leukocyte products,
including lysosomal enzymes and reactive oxygen species, are
secreted and cause tissue injury.
• The mechanism of injury in antibody mediated
glomerulonephritis and many other diseases is inflammation
and leukocyte activation.
• 3)Antibodies that bind to normal cellular receptors or other
proteins may interfere with the functions of these receptors or
proteins and cause disease without inflammation or tissue
damage.
• Antibody-mediated functional abnormalities are the cause of
Graves’ disease and myasthenia gravis.
20. • Antibodies that cause cell- or tissue-specific diseases are
usually auto antibodies produced as part of an autoimmune
reaction against antigens in these cells or tissues.
• Examples of these autoantibodies are listed in Table 18-2.
Less commonly, the antibodies may be produced against a
foreign (e.g., microbial) antigen that is immunologically
cross-reactive with a component of self tissues.
• In a rare sequel of streptococcal infection called rheumatic
fever, antibodies produced against the bacteria cross-react
with antigens in the heart, deposit in this organ, and cause
inflammation and tissue damage.
• Tissue deposits of antibodies may be detected by
morphologic examination in some of these diseases, and
the deposition of antibody is often associated with local
complement activation, inflammation, and tissue injury
21.
22. Experimental Models of Immune
Complex–Mediated Diseases
• Serum Sickness
• analyses of experimental models of serum sickness.
Immunization of an animal such as a rabbit with a
large dose of a foreign protein antigen leads to the
formation of antibodies against the antigen (Fig. 184).
• These antibodies bind to and form complexes with
circulating antigen, which are initially cleared by
macrophages in the liver and spleen.
• As more and more antigen-antibody complexes are
formed, some of them are deposited in vascular
beds.
23. •
•
•
•
•
•
In these tissues, the antibodies in the complexes may activate
complement, with a concomitant fall in serum complement levels.
Complement activation leads to recruitment and activation of
inflammatory cells, predominantly neutrophils, at the sites of immune
complex deposition, and the neutrophils cause tissue injury.
Neutrophils also bind to the immune complexes by their Fcγ receptors,
and Fc receptor signaling activates the leukocytes to produce
substances that damage tissues, as in diseases caused by antibodies
against fixed tissues.
Because the complexes are deposited mainly in small arteries, renal
glomeruli, and the synovia of joints, the clinical and pathologic
manifestations are vasculitis, nephritis, and arthritis.
The clinical symptoms are usually short-lived, and the lesions heal
unless the antigen is injected again. This type of disease is an example
of acute serum sickness.
A more indolent and prolonged disease, called chronic serum sickness,
is produced by multiple injections of antigen, which lead to the
formation of smaller complexes that are deposited most often in the
kidneys, arteries, and lungs.
24. Gell and Coombs Classification
(Type I (IgE-mediated
(Type II (Fc and complement-mediated
(Type III (Immune complex-mediated
(Type IV (Delayed-type hypersensitivity
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•
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25. Type I Hypersensitivity:
History of Discoveries
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•
•
•
Anaphylaxis: Portier and Richet, 1902
Histamine: Dale and Laidlaw, 1911
Transfer of sensitivity: Prausnitz & Küstner
Mast cells as main tissue source of
histamine: Riley and West, 1952
• IgE immunoglobulin: Ishizaka and
Ishizaka, 1966
27. Gell and Coombs Classification
•
•
•
•
Type I (IgE-mediated(
Type II (Fc and complement-mediated(
Type III (Immune complex-mediated(
Type IV (Delayed-type hypersensitivity(
28. Type II Hypersensitivity Reactions:
Mechanisms of Tissue Damage
• Complement-mediated cytolysis
• Antibody-dependent cell-mediated
cytotoxicity (ADCC(
38. Gell and Coombs Classification
•
•
•
•
Type I (IgE-mediated)
Type II (Fc and complement-mediated)
Type III (Immune complex-mediated)
Type IV (Delayed-type hypersensitivity)
39. Type III Hypersensitivity
Mechanisms of Tissue Injury
• In situ activation of complement
• Anaphylatoxin-mediated activation of mast
cells and phagocytes
• Complex-mediated phagocytosis and release
of phagocyte granule enzymes and cytokines
into the local microenvironment
40. Type III Hypersensitivity
Examples of Diseases
• Arthus reaction
• Hypersensitivity pneumonitis
• Immune complex-mediated
glomerulonephritis
• Serum sickness
41. The Arthus Reaction
• Occurs with introduction of antigen into an
individual with high titer antibody
• Requires both complement & phagocytes
• Peaks at 3-6 hours after exposure
• Histology: massive influx of neutrophils, edema,
sometimes necrosis
49. Gell and Coombs Classification
•
•
•
•
Type I (IgE-mediated)
Type II (Fc and complement-mediated)
Type III (Immune complex-mediated)
Type IV (Delayed-type hypersensitivity)
Editor's Notes
Types of antibody-mediated diseases. Antibodies may bind specifically to tissue antigens (A), or they may be deposited
as immune complexes that are formed in the circulation (B). In both cases, the deposited antibodies induce inflammation, leading to tissue injury.
A, Antibodies opsonize cells and may activate complement, generating complement products that also opsonize cells, leading to phagocytosis of the cells through phagocyte Fc receptors or C3 receptors.
B, Antibodies recruit leukocytes by binding to Fc receptors or by activating complement and thereby releasing byproducts that are chemotactic for leukocytes.
Antibodies specific for cell surface receptors for hormones or neurotransmitters may stimulate the activity of the receptors even in the absence of the hormone (left panel) or may inhibit binding of the neurotransmitter to its receptor (right panel). TSH, thyroid stimulating hormone