allergic responses
TRANSCRIPT
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Allergic Responses
Presented by: Kiran Hanif
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Allergic Responses
Also called Hypersensitive responses
Hypersensitive immune reaction to a substance harmless for
healthy individuals.
A type of abnormal immune reaction
Substances induces abnormal immune responses are called
Allergen.
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Atopy
A genetic trait to have a predisposition for localized
anaphylaxis.
Atopic individuals have higher levels of IgE and
eosinophils.
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Genetic Predisposition
Candidate polymorphic genes include:
IL-4 Receptor
IL-4 cytokine (promoter region)
FceRI
Class II MHC (present peptides promoting Th2 response)
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Types of Allergic Reactions
1. Type I or IgE-mediated Hypersensitivity
2. Type II or IgG or IgM-mediated cytotoxic
Hypersensitivity
3. Type III or Complex-mediated Hypersensitivity
4. Type IV or Cell-Mediated Hypersensitivity
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Type I or IgE-mediated Hypersensitivity
Commonly called Allergy
Allergen presented by antigen presenting cells
TH2 cells activate the B cells
B cells give clonal cells
Plasma cells
Memory cells
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Cont……
Plasma cells secreted IgE antibody
Secreted IgE bind to the Fc Receptors
Receptors present on Mast cells & Basophills
Degranulation is induced
Mediators (Histamine) releases
Results in clinical manifestations
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General mechanism showing type I hypersensitivity reaction
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Allergens
Nonparasitic antigens responses capable of
stimulating type I hypersensitivity
Stimulate inappropriate IgE production
Binds to IgE and induces degranulation of cells
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Proteins
• Foreign serum
• Vaccines
Plant pollens
• Rye grass
• Ragweed
• Timothy grass
• Birch trees
Drugs
• Penicillin
• Sulfonamides
• Local anesthetics
• Salicylates
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Foods
• Milk
• Sea Food
• Nuts
Insect products
• Bee venome
• Wasp venom
• Drugs Ant venom
• Cockroach calyx
• Dust mites
Animal hair and dander
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Fc Receptors
Receptors present on the surface of the Mast cells
and Basophills
Two types of Fc receptors are found
High affinity receptor (FcɛRI)
Low-affinity receptor (FcɛRII)
Binding of IgE to receptors induces degranulation
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Structure of high affinity receptor FcɛRI
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Structure of low affinity receptor FcɛRII
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Biochemical events in mast-cell activation and degranulation
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Mediators releases after Degranulation of Mast cells
Mediators are the molecules mediate clinical
menifestations
Pharmacologically active agents act on local tissues
Mediators release induced by allergens results in:
Increase in Vascular permeability
Inflamation
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Classification of Mediators
Classified as:
Primary mediators
Secondary mediators
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Primary Mediators
Histamine
Constriction of smooth muscles.
Bronchiole constriction = wheezing.
Constriction of intestine = cramps-diarrhea.
Vasodilation with increased fluid into tissues causing
increased swelling or fluid in mucosa.
Activates enzymes for tissue breakdown
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Secondary Mediators
Leukotrienes
Prostaglandins
Cytokines
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Effect of mediators
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Phases of type I Hypersensivity reactions
Immediate phase
Involves LTC4 and PGD2
Late phase
Involves IL-4, IL-5, ECF, PAF
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Type I reactions
Type I reactions may be systemic or localized
Systemic anaphylaxis
Localized hypersensitivity reactions
Allergic rhinitis
Food allergies
Asthma
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Asthma
Triggering of disease involve exposure to airborne
& blood-borne allergens such as pollens, dust,
fumes, insects products etc.
Asthematic response can also be divided into:
Early response
Late response
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Early and late responses in asthema
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Effect of degranulation of mast cells in asthema
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Regulation of Type I response
Many factors are responsible for regulating the type
I response which include:
IL-4
IL-5
IL-9
IL-13
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Medical control of Hypersensitivity
Antihistamines
Cromolyn sodium
Theophylline
Epinephrine
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Type II or IgG or IgM-mediated cytotoxic Hypersensitivity
Also called Antibody-mediated cytotoxic
hypersensitivity
Involve antibody-mediated destruction of cells
Antibody bound to a cell surface antigen can
activate complement system
Cell destruction by ADCC
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Type II Reactions
Transfusion reactions
Drug-induced Hemolytic Anemia
Hemolytic disease of Newborn
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Hemolytic disease of the newborn
Also called Erythroblastosis fetalis
Develops when maternal IgG antibodies specific for
fetal blood- group antigens cross the placenta
Destroy fetal red blood cells
Commonly develops when an Rh+ fetus expresses
an Rh antigen on its blood cells
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Type III or Complex-mediated Hypersensitivity
Reaction of antibody with antigen generates
immune complexes
Complexing facilitates the clearance of antigen by
phagocytic cells.
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Effector mechanism
Immune complexes activate the complement system
Anaphylatoxins C3a, C4a, and C5a cause localized
mast-cell degranulation.
C3a, C5a, and C5b67 are also chemotactic factors
for neutrophils
Release of lytic enzymes by neutrophils
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Development of localized type III hypersensitivity
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Type III reactions
Poststreptococcal glomerulonephritis
Rheumatoid arthritis
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Type IV or T Cell-Mediated
Hypersensitivity
TH cells encounter certain types of antigens
Secrete cytokines induces localized inflammatory
reaction
Reactions are delayed by one or more days
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Phases of DTH response
Sensitization phase
begins with an initial contact with an antigen.
Effector phase
subsequent exposure to the antigen
TH1 cells secrete a variety of cytokines
Activate the macrophages
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Phases of type IV hypersensitivity
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Contact dermatitis is type of DTH response
Molecules complex with skin proteins
Complex internalized by skin cells
Processed & presented with MHC II
Results in activation of sensitized TH1 cells
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Development of DTH response after second exposure to
poison oak
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Four types of Allergic responses
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