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Hypersensitivity
Dr. Pavan K.J
➢Hypersensitivity (Immunological reaction) refers to
undesirable immune reactions produced by the normal immune
system.
➢Hypersensitivity reactions: When an immune response result
in exaggerated OR in appropriate reactions harmful to the host
the term hypersensitivity OR allergy used.
➢Hypersensitivity reactions: four types; based on the
mechanisms involved and time taken for the reaction, a
particular clinical condition (disease) may involve more than
one type of reaction.
Hypersensitivity
5
Type I
Type II
Type III
Type IV
Type I, II and III
Type IV
Antibody Mediated
Cell Mediated
6
Classification of Hypersensitivity
Classification of Hypersensitivity
7
 Commonly called allergy
 Mediated by IgE antibodies produced by plasma cells
in response to stimulation of Th2 cells by an
antigens.
 The antigens that stimulate it are called allergens
(i.e. House dust, Pollens, Cosmetics, Insects, Clothing and Drug)
 Exposure may be ingested, inhalation, injection or
direct contact.
 Type I hypersensitivity reactions can be systemic
(e.g., systemic anaphylaxis) or localized to a specific
target tissue or organ (e.g., allergic rhinitis, asthma).
Type I (Immediate) Hypersensitivity
(atopic or anaphylactic)
8
Examples of type I hypersensitivity include:
•allergic asthma
•allergic conjunctivitis eye inflammation caused by an allergic
•allergic rhinitis (‘hay fever’) is a type of inflammation in the nose
•anaphylaxis s a serious allergic reaction that is rapid in onset and may cause death. an
itchy rash, throat or tongue swelling, shortness of breath, vomiting, lightheadedness,
and low blood pressure.
•angio-oedema is painless swelling of submucosal tissues in any part of the body due
to increased vascular permeability.
•atopic dermatitis (eczema) (eczema) is a condition that makes your skin red and itchy.
It's common in children but can occur at any age.
• Eosinophilia is a condition in which the eosinophil count in the peripheral blood
exceeds 5.0×108/l (500/μL). Eosinophils usually account for less than 7% of the
circulating leukocytes.
•Urticaria, also known as hives, is an outbreak of swollen, pale red bumps or plaques
(wheals) on the skin that appear suddenly -- either as a result of the body's reaction to
certain allergens,
Mediator Pharmacological effect
Histamine Vasodilatation, capillary
permeability, bronchoconstriction
Heparin Control of histamine release
Leukotrienes (various) Bronchoconstriction, airway tissue
oedema
Prostaglandins (various) Potent mediators of inflammatory
response
Platelet activating factor Platelet aggregation
Tryptase Proteolytic enzyme activates C3
Kininogenase Kinins → vasodilatation → oedema
Cytokines (IL-5, IL-8, TNFs) Chemoattractants
TABLE 30.14. Mediators of type I hypersensitivity reactions
 Cytotoxic
 Type II hypersensitivity involves IgG or IgM antibody-mediated
 IgM or IgG immunoglobulin react with cell-surface antigens to
activate the complements system and produce direct damage
of the sell surface.
 Transfusion reactions and hemolytic disease of the newborn
are examples of type II hypersensitivity.
Type II (Cytotoxic) Hypersensitivity
9
Hype
rs
e
ns
itivity Type III
Type III (Immune Complex–Mediated) Hypersensitivity
 Type III hypersensitivity is also known as immune complex
hypersensitivity.
 The reaction may take 3 - 10 hours after exposure to the
antigen (as in Arhus reaction).
 The reaction may be general (e.g., serum sickness) or may
involve individual organs including or other organs.
 Antigens causing immune complex mediated injury are:
 Exogenous
 Endogenous
Type III (ICM) Hypersensitivity
11
Mechanism of Type III Hypersensitivity
 Antigens combines with antibody within circulation and form
immune complex
 Wherever in the body they deposited
 They activate compliment system
 Polymorphonuclear cells are attracted to the site
 Result in inflammation and tissue injury
Type III (ICM) Hypersensitivity
12
The mechanism of type III (immune-complex mediated) hypersensitivity-overview
Antigens combine with
antibodies to form
antigen-antibody complexes.
Antigen
Antibody (IgG)
Antigen-antibody complex
Phagocytes remove most
of the complexes, but
some lodge in the walls
of blood vessels.
There the complexes
activate complement.
Inactive complement
Active complement
Antigen-antibodycomplexes
and activated complement
attract and activate
neutrophils, which release
inflammatory chemicals.
Neutrophil
Inflammatory chemicals
Inflammatorychemicals
damage underlying
blood vessel wall.
Type III (ICM) Hypersensitivity
14
Hypersensitivity Type III Reactions
Systemic Reactions
Local Reactions

 ArthusReaction:
It is named for Dr.Arthus.
Inflammation caused by the
deposition of immune
complexes at a localized site.
Clinical Manifestation is :
Hypersensitivity Pneumonitis
 Serum Sickness:
Systemic inflammatory response
to deposited immune complexes at
many areas of body.
Few days to 2 weeks after
injection of foreign serum or drug it
results in :
Fever, Urticaria, Artheralgia,
Eosinophila, Spleenomegally, and
Lymph adenopathy
ImmuneComplex
Diseases
Immune Complex Diseases:




HypersensItIvItyPneumonItIs
GlomerulonephrItIs
RheumatoIdArthritis
SystemIcLupusErythematosus
16
Type III (ICM) Hypersensitivity
Hypersensitivity pneumonitis
Inhalation of antigens into lungs stimulates antibody
production
Subsequent inhalation of the same antigen results in
formation of immune complexes
Activates complement
Type III (ICM) Hypersensitivity
17
Glomerulonephritis
Immune complexes in the blood are deposited in
glomeruli
Damage to the glomerular cells impedes blood
filtration
 Kidney failure and, ultimately, death result
Type III (ICM) Hypersensitivity
18
Rheumatoid arthritis
 Immune complexes deposited in the joint
Results in release of inflammatory chemicals
The joints begin to break down and become
distorted
 Trigger not well understood
 Treated with anti-inflammatory drugs
Type III (ICM) Hypersensitivity
19
The crippling distortion of joints characteristic of rheumatoid arthritis
Systemic lupus erythematosus
Autoantibodies against DNA result in immune
complex formation
Many other autoantibodies can also occur
Against red blood cells, platelets, lymphocytes,
muscle cells
Trigger unknown
 Immunosuppressive drugs reduce autoantibody
formation
Glucocorticoids reduce inflammation
Type III (ICM) Hypersensitivity
21
The characteristic facial rash of systemic lupus erythematosus
Hype
rs
e
ns
itivity Type IV
Type IV (Cell Mediated) Hypersensitivity
Type IV (Delayed or Cell-Mediated) Hypersensitivity
 Delayed hypersensitivity is a function of T Lymphocytes, not
antibody.
 It starts hours (or Days) after contact with the antigen and often
lasts for days.
 It can be transferred by immunologically committed
(Sensitized) T cells, not by serum.
 Principal pattern of immunologic response to variety of intra
cellular microbiologic agents
i.e.: Mycobacterium Tuberculosis
Viruses
Fungi
Parasites
24
Mechanism of Type IV Hypersensitivity
 Activated T Lymphocytes


Release of cytokines and macrophage activation
T-cell mediated cytotoxicity
25
Type IV (Cell Mediated) Hypersensitivity
2
6
Type IV (Cell Mediated) Hypersensitivity
Clinically
Important
DelayedHypersensitivityReactions
The tuberculin response
 An injection of tuberculin beneath the skin causes
reaction in individual exposed to tuberculosis or
tuberculosis vaccine
 Used to diagnose contact with antigens of
M. tuberculosis
No response when individual not infected or
vaccinated
Red, hard swelling develops in individuals
previously infected or immunized
Type IV (Cell Mediated) Hypersensitivity
28
A positive tuberculin test
Allergic contact dermatitis
 Cell-mediated immune response
 Results in an intensely irritating skin rash
 Triggered by chemically modified skin proteins that
the body regards as foreign
 Acellular, fluid-filled blisters develop in severe cases
 Can be treated with glucocorticoids
Type IV (Cell Mediated) Hypersensitivity
30
Allergic contact dermatitis
Type IV (Cell Mediated) Hypersensitivity
• Graft rejection
 Rejection of tissues or organs that
have been transplanted
 Grafts perceived as foreign by a recipient
undergo rejection
 Immune response against foreign MHC on
graft cells
 Rejection depends on degree to which the
graft is foreign to the recipient
•Based on the type of graft 32
Types of grafts
Autograft
Isograft Xenograft
Genetically identical
sibling or clone
Allograft
Genetically different
member of same species
Hypersensitivity Reactions Conclusion:
34
 Books:
 Review of Medical Microbiology and Immunology
(Warren Levinson)
(Carol Mattson Porth)
(Robins)

 Pathophysiology
 Basic Pathology
Internet:
 www. pathmicro.med.sc.edu
 www. en.wikipedia.org
 www. inkling.com
 www. medical-dictionary.thefreedictionary.com
35
References:
Questions
36
37

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Hypersensitivity

  • 2. ➢Hypersensitivity (Immunological reaction) refers to undesirable immune reactions produced by the normal immune system. ➢Hypersensitivity reactions: When an immune response result in exaggerated OR in appropriate reactions harmful to the host the term hypersensitivity OR allergy used. ➢Hypersensitivity reactions: four types; based on the mechanisms involved and time taken for the reaction, a particular clinical condition (disease) may involve more than one type of reaction. Hypersensitivity 5
  • 3. Type I Type II Type III Type IV Type I, II and III Type IV Antibody Mediated Cell Mediated 6 Classification of Hypersensitivity
  • 5.  Commonly called allergy  Mediated by IgE antibodies produced by plasma cells in response to stimulation of Th2 cells by an antigens.  The antigens that stimulate it are called allergens (i.e. House dust, Pollens, Cosmetics, Insects, Clothing and Drug)  Exposure may be ingested, inhalation, injection or direct contact.  Type I hypersensitivity reactions can be systemic (e.g., systemic anaphylaxis) or localized to a specific target tissue or organ (e.g., allergic rhinitis, asthma). Type I (Immediate) Hypersensitivity (atopic or anaphylactic) 8
  • 6. Examples of type I hypersensitivity include: •allergic asthma •allergic conjunctivitis eye inflammation caused by an allergic •allergic rhinitis (‘hay fever’) is a type of inflammation in the nose •anaphylaxis s a serious allergic reaction that is rapid in onset and may cause death. an itchy rash, throat or tongue swelling, shortness of breath, vomiting, lightheadedness, and low blood pressure. •angio-oedema is painless swelling of submucosal tissues in any part of the body due to increased vascular permeability. •atopic dermatitis (eczema) (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. • Eosinophilia is a condition in which the eosinophil count in the peripheral blood exceeds 5.0×108/l (500/μL). Eosinophils usually account for less than 7% of the circulating leukocytes. •Urticaria, also known as hives, is an outbreak of swollen, pale red bumps or plaques (wheals) on the skin that appear suddenly -- either as a result of the body's reaction to certain allergens,
  • 7. Mediator Pharmacological effect Histamine Vasodilatation, capillary permeability, bronchoconstriction Heparin Control of histamine release Leukotrienes (various) Bronchoconstriction, airway tissue oedema Prostaglandins (various) Potent mediators of inflammatory response Platelet activating factor Platelet aggregation Tryptase Proteolytic enzyme activates C3 Kininogenase Kinins → vasodilatation → oedema Cytokines (IL-5, IL-8, TNFs) Chemoattractants TABLE 30.14. Mediators of type I hypersensitivity reactions
  • 8.
  • 9.  Cytotoxic  Type II hypersensitivity involves IgG or IgM antibody-mediated  IgM or IgG immunoglobulin react with cell-surface antigens to activate the complements system and produce direct damage of the sell surface.  Transfusion reactions and hemolytic disease of the newborn are examples of type II hypersensitivity. Type II (Cytotoxic) Hypersensitivity 9
  • 10.
  • 11.
  • 13. Type III (Immune Complex–Mediated) Hypersensitivity  Type III hypersensitivity is also known as immune complex hypersensitivity.  The reaction may take 3 - 10 hours after exposure to the antigen (as in Arhus reaction).  The reaction may be general (e.g., serum sickness) or may involve individual organs including or other organs.  Antigens causing immune complex mediated injury are:  Exogenous  Endogenous Type III (ICM) Hypersensitivity 11
  • 14. Mechanism of Type III Hypersensitivity  Antigens combines with antibody within circulation and form immune complex  Wherever in the body they deposited  They activate compliment system  Polymorphonuclear cells are attracted to the site  Result in inflammation and tissue injury Type III (ICM) Hypersensitivity 12
  • 15. The mechanism of type III (immune-complex mediated) hypersensitivity-overview Antigens combine with antibodies to form antigen-antibody complexes. Antigen Antibody (IgG) Antigen-antibody complex Phagocytes remove most of the complexes, but some lodge in the walls of blood vessels. There the complexes activate complement. Inactive complement Active complement Antigen-antibodycomplexes and activated complement attract and activate neutrophils, which release inflammatory chemicals. Neutrophil Inflammatory chemicals Inflammatorychemicals damage underlying blood vessel wall.
  • 16. Type III (ICM) Hypersensitivity 14 Hypersensitivity Type III Reactions Systemic Reactions Local Reactions   ArthusReaction: It is named for Dr.Arthus. Inflammation caused by the deposition of immune complexes at a localized site. Clinical Manifestation is : Hypersensitivity Pneumonitis  Serum Sickness: Systemic inflammatory response to deposited immune complexes at many areas of body. Few days to 2 weeks after injection of foreign serum or drug it results in : Fever, Urticaria, Artheralgia, Eosinophila, Spleenomegally, and Lymph adenopathy
  • 19. Hypersensitivity pneumonitis Inhalation of antigens into lungs stimulates antibody production Subsequent inhalation of the same antigen results in formation of immune complexes Activates complement Type III (ICM) Hypersensitivity 17
  • 20. Glomerulonephritis Immune complexes in the blood are deposited in glomeruli Damage to the glomerular cells impedes blood filtration  Kidney failure and, ultimately, death result Type III (ICM) Hypersensitivity 18
  • 21. Rheumatoid arthritis  Immune complexes deposited in the joint Results in release of inflammatory chemicals The joints begin to break down and become distorted  Trigger not well understood  Treated with anti-inflammatory drugs Type III (ICM) Hypersensitivity 19
  • 22. The crippling distortion of joints characteristic of rheumatoid arthritis
  • 23. Systemic lupus erythematosus Autoantibodies against DNA result in immune complex formation Many other autoantibodies can also occur Against red blood cells, platelets, lymphocytes, muscle cells Trigger unknown  Immunosuppressive drugs reduce autoantibody formation Glucocorticoids reduce inflammation Type III (ICM) Hypersensitivity 21
  • 24. The characteristic facial rash of systemic lupus erythematosus
  • 26. Type IV (Cell Mediated) Hypersensitivity Type IV (Delayed or Cell-Mediated) Hypersensitivity  Delayed hypersensitivity is a function of T Lymphocytes, not antibody.  It starts hours (or Days) after contact with the antigen and often lasts for days.  It can be transferred by immunologically committed (Sensitized) T cells, not by serum.  Principal pattern of immunologic response to variety of intra cellular microbiologic agents i.e.: Mycobacterium Tuberculosis Viruses Fungi Parasites 24
  • 27. Mechanism of Type IV Hypersensitivity  Activated T Lymphocytes   Release of cytokines and macrophage activation T-cell mediated cytotoxicity 25 Type IV (Cell Mediated) Hypersensitivity
  • 28. 2 6 Type IV (Cell Mediated) Hypersensitivity
  • 30. The tuberculin response  An injection of tuberculin beneath the skin causes reaction in individual exposed to tuberculosis or tuberculosis vaccine  Used to diagnose contact with antigens of M. tuberculosis No response when individual not infected or vaccinated Red, hard swelling develops in individuals previously infected or immunized Type IV (Cell Mediated) Hypersensitivity 28
  • 32. Allergic contact dermatitis  Cell-mediated immune response  Results in an intensely irritating skin rash  Triggered by chemically modified skin proteins that the body regards as foreign  Acellular, fluid-filled blisters develop in severe cases  Can be treated with glucocorticoids Type IV (Cell Mediated) Hypersensitivity 30
  • 34. Type IV (Cell Mediated) Hypersensitivity • Graft rejection  Rejection of tissues or organs that have been transplanted  Grafts perceived as foreign by a recipient undergo rejection  Immune response against foreign MHC on graft cells  Rejection depends on degree to which the graft is foreign to the recipient •Based on the type of graft 32
  • 35. Types of grafts Autograft Isograft Xenograft Genetically identical sibling or clone Allograft Genetically different member of same species
  • 37.  Books:  Review of Medical Microbiology and Immunology (Warren Levinson) (Carol Mattson Porth) (Robins)   Pathophysiology  Basic Pathology Internet:  www. pathmicro.med.sc.edu  www. en.wikipedia.org  www. inkling.com  www. medical-dictionary.thefreedictionary.com 35 References:
  • 39. 37