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HYPERSENSITIVITY
Hypersensitivity 
• Hypersensitivity (also called hypersensitivity 
reaction or intolerance) refers to excessive, undesirable 
(damaging, discomfort-producing and sometimes fatal) reactions 
produced by the normal immune system. 
• Hypersensitivity reactions require a pre-sensitized (immune) state of 
the host. 
Hypersensitivity Types 
• On the basis of mechanisms involved and time taken for the reaction, 
hypersensitivity reactions can be divided into four types: 
I. type I 
II. type II 
III. type III 
IV. type IV
Type I hypersensitivity 
• Type I hypersensitivity is also known as immediate or anaphylactic 
hypersensitivity.It develops within few minutes of exposure to an allergen. 
• Anaphylactic reactions are mediated by IgE and other factors involved in 
inflammation (inflammation means the protective response of the tissues to 
the damage or destruction of cells). When the body is exposed to an allergen, 
the IgE immunoglobulins are produced. 
• These immunoglobulins bind with the surface receptors of mast cells and 
circulating basophils. 
• Mast cells are the granulated wandering cells found in connective tissue and 
beneath the mucous membrane in the throat, lungs and eyes. 
• During subsequent exposure of the body to the same allergen, the allergen 
IgE antibody reaction takes place. 
• This leads to degranulation of mast cells and basophils, with the release of 
some chemical mediators such histamine. The chemical mediators produce 
the hypersensitivity reactions. 
• Most serious reactions are fall in blood pressure (due to 
vasodilatation),obstruction of air passage and difficulty in breathing (due to 
bronchoconstriction) and shock
Anaphylactic and anaphylactoid reaction 
• The reaction is systemic, which involves multiple organ systems, and 
is a direct result of the release of chemical mediators from mast cells 
and basophils. 
• Specifically, the condition anaphylaxis requires the patient to be 
sensitized, and their reaction mediated through IgE antibodies. An 
anaphylactoid reaction doesn’t need the presence of IgE antibodies 
for a hypersensitivity reaction to occur. 
• Substances initiating the anaphylactoid reaction, such as radiopaque 
contrast media, nonsteroidal anti-inflammatory drugs (NSAIDs) and 
aspirin cause a direct breakdown of the mast cell and basophil 
membranes. 
• Thus, an anaphylactic reaction occurs only after the patient has been 
previously exposed at least once to the antigen and is sensitized; an 
anaphylactoid reaction can occur following a single, first-time 
exposure to certain agents in nonsensitized patients.
Diagnosis and Treatment 
• Diagnostic tests for immediate hypersensitivity include skin (prick 
and intradermal) tests, 
• measurement of total IgE and specific IgE antibodies against the 
suspected allergens. Increased IgE levels are indicative of an atopic 
condition, 
• Symptomatic treatment is achieved with antihistamines which block 
histamine receptors. Chromolyn sodium inhibits mast cell 
degranulation, 
• Hyposensitization (immunotherapy or desensitization) is another 
treatment which is successful in a number of allergies, particularly 
to insect venoms 
• The primary treatment of anaphylaxis is injection 
of epinephrine, the administration of intravenous fluids, and 
positioning the person flat
Type II hypersensitivity 
• Type II hypersensitivity is also known as cytotoxic hypersensitivity and 
may affect a variety of organs and tissues. 
• The antigens are normally endogenous, although exogenous chemicals 
(haptens) that can attach to cell membranes can also lead to type II 
hypersensitivity. 
• Drug-induced hemolytic anemia, granulocytopenia and 
thrombocytopenia are such examples. 
• The reaction time is minutes to hours. 
• Type 11 reactions involve the activation of complement by the 
combination of IgM or IgG antibodies with an antigenic cell. 
• This activation stimulates the complement to lyse the affected 
cell,which might be either a host cell or foreign cell that carries a 
foreign antigenic determinant (such as a drug)on its surface.
• Additional cellular damage may be caused within 5-8 
hours by the action of macrophages and other cells that 
attack antibody –coated cell. 
• Eg. Transfusion reactions, in which red blood cells are 
destroyed as a result of reacting with circulating 
antibodies.These involve blood group system 
Diagnosis and treatment 
Diagnostic tests include detection of circulating antibody against 
the tissues involved by immunofluorescence 
• Staning procedures also used in diagnosis 
• Treatment involves anti-inflammatory and immunosuppressive 
agents.
TYPE III HYPERSENSITIVITY 
• Type III hypersensitivity is also known as Arthus or 
immune complex hypersensitivity. The reaction may be 
general (e.g., serum sickness) or may involve individual 
organs including skin (e.g., systemic lupus erythematosus, 
reaction), kidneys (e.g., lupus nephritis) joints (e.g., 
rheumatoid arthritis) or other organs. 
• The reaction may take 3 - 10 hours after exposure to the 
antigen. 
• Excess amounts of antibodies like IgG or IgM are 
produced in this type. The antigen-antibody complexes 
are precipitated and deposited in localized areas like 
joints causing arthritis, heart causing myocarditis and 
glomeruli of kidney producing glomerulonephritis.
Diagnosis and treatment 
• Diagnosis involves examination of tissue biopsies for deposits 
of Ig and complement by immunofluorescence. 
• Treatment includes anti-inflammatory agents.
Type IV hypersensitivity 
• Type IV hypersensitivity is also known as cell mediated or delayed type 
hypersensitivity. 
• The classical example of this hypersensitivity is tuberculin (Montoux) 
reaction which peaks 48 hours after the injection of antigen (tuberculin) 
• Mechanisms of damage in delayed hypersensitivity include T lymphocytes 
and monocytes and/or macrophages. 
There are two different types of reactions capable of causing 
tissue injury in this way. 
1.delayed type hypersensitivity is mediated by CD4+ helper T 
cells 
2. cell mediated cytotoxicity, is mediated by CD8+ T cells. 
• Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells 
secrete cytokines which activate cytotoxic T cells and recruit and activate 
monocytes and macrophages, which cause the damage. 
• The delayed hypersensitivity lesions mainly contain monocytes and a few T 
cells.
Diagnosis and treatment 
• Diagnostic tests include 
• Montoux test 
• patch test (for contact dermatitis) 
• mitogenic response 
• IL-2 production. 
• Corticosteroids and other immunosuppressive agents are used in 
treatment.
Table - Comparison of Different Types of hypersensitivity 
characteristics 
type-I 
(anaphylactic) 
type-II 
(cytotoxic) 
type-III 
(immune complex) 
type-IV 
(delayed type) 
antibody IgE IgG, IgM IgG, IgM None 
antigen exogenous cell surface soluble tissues & organs 
response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours 
appearance weal & flare lysis and necrosis 
erythema and 
edema, necrosis 
erythema and 
induration 
transferred with antibody antibody antibody T-cells 
examples 
allergic asthma, 
hay fever 
erythroblastosis 
fetalis, 
SLE, 
tuberculin test, 
poison ivy, 
granuloma
•A tuberculin skin test (also called a Mantoux 
tuberculin test) is done to diagnose tuberculosis (TB). The 
test is done by putting a small amount of TB protein 
(antigens) under the top layer of skin on your inner forearm. 
If you have ever been exposed to the TB bacteria 
(Mycobacterium tuberculosis), your skin will react to the 
antigens by developing a firm red bump at the site within 2 
days.
Hypersensitivity PPT

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Hypersensitivity PPT

  • 2. Hypersensitivity • Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. • Hypersensitivity reactions require a pre-sensitized (immune) state of the host. Hypersensitivity Types • On the basis of mechanisms involved and time taken for the reaction, hypersensitivity reactions can be divided into four types: I. type I II. type II III. type III IV. type IV
  • 3. Type I hypersensitivity • Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.It develops within few minutes of exposure to an allergen. • Anaphylactic reactions are mediated by IgE and other factors involved in inflammation (inflammation means the protective response of the tissues to the damage or destruction of cells). When the body is exposed to an allergen, the IgE immunoglobulins are produced. • These immunoglobulins bind with the surface receptors of mast cells and circulating basophils. • Mast cells are the granulated wandering cells found in connective tissue and beneath the mucous membrane in the throat, lungs and eyes. • During subsequent exposure of the body to the same allergen, the allergen IgE antibody reaction takes place. • This leads to degranulation of mast cells and basophils, with the release of some chemical mediators such histamine. The chemical mediators produce the hypersensitivity reactions. • Most serious reactions are fall in blood pressure (due to vasodilatation),obstruction of air passage and difficulty in breathing (due to bronchoconstriction) and shock
  • 4. Anaphylactic and anaphylactoid reaction • The reaction is systemic, which involves multiple organ systems, and is a direct result of the release of chemical mediators from mast cells and basophils. • Specifically, the condition anaphylaxis requires the patient to be sensitized, and their reaction mediated through IgE antibodies. An anaphylactoid reaction doesn’t need the presence of IgE antibodies for a hypersensitivity reaction to occur. • Substances initiating the anaphylactoid reaction, such as radiopaque contrast media, nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin cause a direct breakdown of the mast cell and basophil membranes. • Thus, an anaphylactic reaction occurs only after the patient has been previously exposed at least once to the antigen and is sensitized; an anaphylactoid reaction can occur following a single, first-time exposure to certain agents in nonsensitized patients.
  • 5.
  • 6. Diagnosis and Treatment • Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, • measurement of total IgE and specific IgE antibodies against the suspected allergens. Increased IgE levels are indicative of an atopic condition, • Symptomatic treatment is achieved with antihistamines which block histamine receptors. Chromolyn sodium inhibits mast cell degranulation, • Hyposensitization (immunotherapy or desensitization) is another treatment which is successful in a number of allergies, particularly to insect venoms • The primary treatment of anaphylaxis is injection of epinephrine, the administration of intravenous fluids, and positioning the person flat
  • 7. Type II hypersensitivity • Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. • The antigens are normally endogenous, although exogenous chemicals (haptens) that can attach to cell membranes can also lead to type II hypersensitivity. • Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. • The reaction time is minutes to hours. • Type 11 reactions involve the activation of complement by the combination of IgM or IgG antibodies with an antigenic cell. • This activation stimulates the complement to lyse the affected cell,which might be either a host cell or foreign cell that carries a foreign antigenic determinant (such as a drug)on its surface.
  • 8. • Additional cellular damage may be caused within 5-8 hours by the action of macrophages and other cells that attack antibody –coated cell. • Eg. Transfusion reactions, in which red blood cells are destroyed as a result of reacting with circulating antibodies.These involve blood group system Diagnosis and treatment Diagnostic tests include detection of circulating antibody against the tissues involved by immunofluorescence • Staning procedures also used in diagnosis • Treatment involves anti-inflammatory and immunosuppressive agents.
  • 9. TYPE III HYPERSENSITIVITY • Type III hypersensitivity is also known as Arthus or immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, reaction), kidneys (e.g., lupus nephritis) joints (e.g., rheumatoid arthritis) or other organs. • The reaction may take 3 - 10 hours after exposure to the antigen. • Excess amounts of antibodies like IgG or IgM are produced in this type. The antigen-antibody complexes are precipitated and deposited in localized areas like joints causing arthritis, heart causing myocarditis and glomeruli of kidney producing glomerulonephritis.
  • 10. Diagnosis and treatment • Diagnosis involves examination of tissue biopsies for deposits of Ig and complement by immunofluorescence. • Treatment includes anti-inflammatory agents.
  • 11. Type IV hypersensitivity • Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. • The classical example of this hypersensitivity is tuberculin (Montoux) reaction which peaks 48 hours after the injection of antigen (tuberculin) • Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. There are two different types of reactions capable of causing tissue injury in this way. 1.delayed type hypersensitivity is mediated by CD4+ helper T cells 2. cell mediated cytotoxicity, is mediated by CD8+ T cells. • Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the damage. • The delayed hypersensitivity lesions mainly contain monocytes and a few T cells.
  • 12.
  • 13. Diagnosis and treatment • Diagnostic tests include • Montoux test • patch test (for contact dermatitis) • mitogenic response • IL-2 production. • Corticosteroids and other immunosuppressive agents are used in treatment.
  • 14. Table - Comparison of Different Types of hypersensitivity characteristics type-I (anaphylactic) type-II (cytotoxic) type-III (immune complex) type-IV (delayed type) antibody IgE IgG, IgM IgG, IgM None antigen exogenous cell surface soluble tissues & organs response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours appearance weal & flare lysis and necrosis erythema and edema, necrosis erythema and induration transferred with antibody antibody antibody T-cells examples allergic asthma, hay fever erythroblastosis fetalis, SLE, tuberculin test, poison ivy, granuloma
  • 15. •A tuberculin skin test (also called a Mantoux tuberculin test) is done to diagnose tuberculosis (TB). The test is done by putting a small amount of TB protein (antigens) under the top layer of skin on your inner forearm. If you have ever been exposed to the TB bacteria (Mycobacterium tuberculosis), your skin will react to the antigens by developing a firm red bump at the site within 2 days.