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PRESENTED BY
SAPNITA SHINDE
© Sapnita Shinde, 2020
Hypersensitivity- refers to undesirable reactions
produced by the normal immune system, including
allergies and autoimmunity.
•These reactions may be damaging, uncomfortable,or occasionally fatal.
•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.
Atopy-a hereditary predisposition to the development of immediate hypersensitivity
against common environmental antigens.
•Atopic individuals have higher levels of IgE and eosinophils.
Charles Richet-Noble Prize
in 1913 for his work in
anaphylaxis.
Paul Portier
HISTORY-
Gell and Coombs Classification-
TYPE 1-HYPERSENSITIVITY
 Type I hypersensitivity is also known as immediate or
anaphylactic hypersensitivity.
 The reaction may involve skin (urticaria and eczema), eyes
(conjunctivitis), nasopharynx (rhinorrhea, rhinitis),
bronchopulmonary tissues (asthma) and gastrointestinal
tract (gastroenteritis)
 The reaction may cause a range of symptoms from minor
inconvenience to death.
 The reaction usually takes 15 - 30 minutes from the time of
exposure to the antigen.
 sometimes it may have a delayed onset (10 - 12 hours).
Common allergens-
Fc€RI andFc€RII receptors-
ITAM-immunoreceptor tyrosine
based activation motif
Overview of Biochemical events In
mast cell and degranulation- PIP2-phosphatidylinositol4,5bispho
PS-Phosphatidyl serine
PE-Phatidylethanolamine
Some examples:
 Allergic asthma
 Allergic conjunctivitis
 Allergic rhinitis ("hay fever")
 Anaphylaxis-inc.vascular permeability
 Angioedema
 Urticaria (hives)
Urticaria(hives)
TREATMENT-
Antihistamines-decreases vascular permeability and
Bronchoconstriction.
Corticosteroids-decreases inflammatory response.
Epinephrine-constrict Blood vessels (PREVENT anaphylactic
shock)
Intravascular injection through Epi Pen.
Intravenous injection.
TYPE II HYPERSENSITIVITY
 Type II hypersensitivity is also known as cytotoxic
hypersensitivity and may affect a variety of organs
and tissues.This is IgM or IgG Ab Mediated.
 The antigens are normally endogenous, although
exogenous chemicals (haptens) which can attach to
cell membranes can also lead to type II
hypersensitivity.
 Antibody mediated destruction of cell.
Examples:
- Drug-induced hemolytic anemia
-Granulocytopenia
-Thrombocytopenia
MECHANISM-
Myasthenia
Gravis
Examples-
 Haemolytic anaemia
Immune thrombocytopenia
• Good pastures syndrome.
 Myasthenia gravis
 Hemolytic disease
of the new born.
 Farmer’s Lung.
 Graves Disease.
Coombs Test-
TYPE III HYPERSENSITIVITY
 Also known as immune complex disease
 occurs when immune complex (Ag-Ab) are not
removed from circulation
 These complexes are deposited in various tissues
and organs such as:
- Kidneys
- Joints
- Lung
- Skin
MECHANISM-
MECHANISM
Step 1
Large quantities of
soluble antigen-
antibody complexes
form in the blood and
are not completely
removed by
macrophages.
Step 2
These antigen-
antibody complexes
lodge in the
capillaries between
the endothelial cells
and the basement
membrane.
Step 3
These antigen-
antibody complexes
activate the classical
complement
pathway leading to
vasodilatation.
Step 4
The complement proteins and antigen-antibody complexes
attract leukocytes to the area.
Step 5 The leukocytes
discharge their
killing agents and
promote massive
inflammation. This
can lead to tissue
death and
hemorrhage.
Examples:
 Immune complex glomerulonephritis
 Rheumatoid arthritis
 Serum sickness
 Symptoms of malaria
 Systemic lupus erythematosus
 Arthus reaction
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
 Reaction peaks 48 hours after the injection of
antigen. The lesion is characterized by induration
and erythema
A Positive Tuberculin test-
 Type IV hypersensitivity is involved in the pathogenesis of many
autoimmune and infectious diseases:
 Tuberculosis
 Leprosy
 Multiple Sclerosis-myelin around nerve fibres.
 Inflammatory Bowel Disease –lining of Intestine
 Hashimoto Thyroditis-attack thyroid epithelial cell
Type1-Diabetes Melitus
Diagnosis
 Diagnostic tests in vivo include delayed cutaneous
reaction (e.g. Montoux test )
 In vitro tests for delayed hypersensitivity include
mitogenic response, lympho-cytotoxicity and IL-2
production.
 Corticosteroids & other immunosuppressive agents
are used in treatment.
Induration
THANKYOU

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Hypersensitivity Types and Mechanisms

  • 1. PRESENTED BY SAPNITA SHINDE © Sapnita Shinde, 2020
  • 2. Hypersensitivity- refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. •These reactions may be damaging, uncomfortable,or occasionally fatal. •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. Atopy-a hereditary predisposition to the development of immediate hypersensitivity against common environmental antigens. •Atopic individuals have higher levels of IgE and eosinophils.
  • 3. Charles Richet-Noble Prize in 1913 for his work in anaphylaxis. Paul Portier HISTORY-
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  • 5. Gell and Coombs Classification-
  • 6. TYPE 1-HYPERSENSITIVITY  Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity.  The reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis)  The reaction may cause a range of symptoms from minor inconvenience to death.  The reaction usually takes 15 - 30 minutes from the time of exposure to the antigen.  sometimes it may have a delayed onset (10 - 12 hours).
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  • 9. Fc€RI andFc€RII receptors- ITAM-immunoreceptor tyrosine based activation motif
  • 10. Overview of Biochemical events In mast cell and degranulation- PIP2-phosphatidylinositol4,5bispho PS-Phosphatidyl serine PE-Phatidylethanolamine
  • 11. Some examples:  Allergic asthma  Allergic conjunctivitis  Allergic rhinitis ("hay fever")  Anaphylaxis-inc.vascular permeability  Angioedema  Urticaria (hives) Urticaria(hives)
  • 12. TREATMENT- Antihistamines-decreases vascular permeability and Bronchoconstriction. Corticosteroids-decreases inflammatory response. Epinephrine-constrict Blood vessels (PREVENT anaphylactic shock) Intravascular injection through Epi Pen. Intravenous injection.
  • 13. TYPE II HYPERSENSITIVITY  Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues.This is IgM or IgG Ab Mediated.  The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity.  Antibody mediated destruction of cell. Examples: - Drug-induced hemolytic anemia -Granulocytopenia -Thrombocytopenia
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  • 16. Examples-  Haemolytic anaemia Immune thrombocytopenia • Good pastures syndrome.  Myasthenia gravis  Hemolytic disease of the new born.  Farmer’s Lung.  Graves Disease.
  • 18. TYPE III HYPERSENSITIVITY  Also known as immune complex disease  occurs when immune complex (Ag-Ab) are not removed from circulation  These complexes are deposited in various tissues and organs such as: - Kidneys - Joints - Lung - Skin
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  • 23. MECHANISM Step 1 Large quantities of soluble antigen- antibody complexes form in the blood and are not completely removed by macrophages.
  • 24. Step 2 These antigen- antibody complexes lodge in the capillaries between the endothelial cells and the basement membrane.
  • 25. Step 3 These antigen- antibody complexes activate the classical complement pathway leading to vasodilatation.
  • 26. Step 4 The complement proteins and antigen-antibody complexes attract leukocytes to the area.
  • 27. Step 5 The leukocytes discharge their killing agents and promote massive inflammation. This can lead to tissue death and hemorrhage.
  • 28. Examples:  Immune complex glomerulonephritis  Rheumatoid arthritis  Serum sickness  Symptoms of malaria  Systemic lupus erythematosus  Arthus reaction
  • 29. 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  Reaction peaks 48 hours after the injection of antigen. The lesion is characterized by induration and erythema
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  • 32.  Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases:  Tuberculosis  Leprosy  Multiple Sclerosis-myelin around nerve fibres.  Inflammatory Bowel Disease –lining of Intestine  Hashimoto Thyroditis-attack thyroid epithelial cell
  • 34. Diagnosis  Diagnostic tests in vivo include delayed cutaneous reaction (e.g. Montoux test )  In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production.  Corticosteroids & other immunosuppressive agents are used in treatment.