Hypersensitivity Reactions Flashcards
Inappropriate/ exaggerated immune responses to •Harmless environmental antigens •Infections •Auto-antigens
causing tissue damage.
Is?
Hypersensitivity
Four types according to mechanism of tissue damage ?
Type I (Immediate/ anaphylactic) “IgE- mediated” • Type II (cytolytic) ”IgG/ IgM - mediated”
Type III (immune-complex mediated) ”IgG/IgM-mediated
Type IV (delayed /cell-mediated)
Exaggerated immune responses to harmless environmental antigens (allergens).
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Type “I” hypersensitivity
Immediate/Anaphylactic
Mediated by IgE ?
Type “I” hypersensitivity
Immediate / anaphylactic
degranulation of Mast cells and eosinophils ?
Type “I” hypersensitivity
Immediate/ anaphylactic
ffects are felt within minutes of exposure
Type “I” hypersensitivity
immediate hypersensitivity”
Type” I” hypersensitivity
Mechanism: ?
A- Sensitization (1st Exposure):
B- Re-exposure to the same allergen:
Type” I” hypersensitivity
Mechanism: A- Sensitization (1st Exposure): Normally, antigenic stimulation ? And condition ?
production of extremely low levels of IgE.
Certain individuals have a genetic predisposition to allergy, respond to certain antigens (allergens) by forming large amounts of IgE. ●IgE molecules bind to Fc receptors on mast cells & basophils
●Thus, 1st exposure to an allergen →
sensitization of Mast cells & Basophils
1st exposure to an allergen →
sensitization of ?
Mast cells & Basophils
Type “I” hypersensitivity
Mechanism: B- Re-exposure to the same allergen: ?
Antigen binds 2 adjacent IgE molecules on mast cells (cross-linking) → Degranulation of mast cells “release granules and mediators”.
Degranulation: release 2 kinds of mediators:
• Preformed mediators:
◦
Histamine and platelet activating factor (PAF)
Which type of hypersensitivity and clinical form? symptoms are localized in one organ or system Urticaria (+ itching) Gastrointestinal symptoms
Bronchial asthma
Type “I” hypersensitivity Clinical Forms
1. Localized form (Atopy):
Type and clinical form? insect venom (e.g., honey bee sting) Symptoms: ● Itching, severe bronchoconstriction and hypotension
shock
Type “I” hypersensitivity Clinical Forms
II. Systemic anaphylaxis:
Detection of the antigen to which the individual is sensitive
extracts of various antigens are introduced into the skin of the patient.
Positive cases show
a wheal and flare reaction that appears
within 15-25 min.
Type “I” hypersensitivity Diagnosis
1- Skin test:
Type “I” hypersensitivity Diagnosis through ?
1- Skin test
2- Measurement of serum levels of total IgE and IgE specific for a particular allergen.
Mediated by IgG / IgM antibodies reacting with Cell-bound antigen (surface antigen).
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Type “II” hypersensitivity / cytolytic / cytotoxic
Mechanism of tissue damage 1. Complement activation
➢Lysis of target cells
2. Antibody-dependent cell-mediated cytotoxicity (ADCC) through the action of natural killer (NK) cells.
3. Opsonization of target cells
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Type “II” hypersensitivity Mechanism
Cytotoxic/ cytolytic
Type of hypersensitivity? Transfusion reactions (Blood group ABO incompatibility).
Type 2 cytotoxic
Hemolytic disease of the newborn (Rh incompatibility)
Type of hypersensitivity?
Type 2 cytotoxic
A drug may become attached to a cell surface (e.g., RBCs/platelets) Antibodies to the drug reacting at the cell surface lead to destruction of the cell in presence of complement
Type hypersensitivity?
Type 2 hypersensitivity
Autoimmune diseases
e.g., Autoimmune hemolytic anemia
(autoantibodies to an individual’s own red blood cells)
Gave’s Disease (antibodies against TSH receptors”agonist effect”)
4. Graft rejection
Type of hypersensitivity?
Type 2 cytotoxic
When antibodies combine with their specific antigen,
immune complexes are formed
Type of reaction ?
Type “III” hypersensitivity IMMUNE-COMPLEX
Antibodies (IgG or IgM) formed against ?
Type “III” hypersensitivity immune complex
Formation of soluble immune complexes antigen and IgG / IgM.
Immune complexes penetrate the endothelium of blood vessel walls & become deposited on the vascular basement membrane.
Complement is activated
& C3a and C5a (anaphylatoxins) are released Platelets are aggregated →
Type of hypersensitivity?
Type “III” hypersensitivity immune complex
Post-streptococcal glomerulonephritis / Autoimmune diseases e.g., SLE (systemic lupus erythematosis) / Graft rejection
Ex of ?
Type “III” hypersensitivity / immune complex
Exaggerated cell-mediated immune response ?
Type “IV” hypersensitivity : delayed
Antibodies have NO role
The main cell involved is the activated Th1
Type “IV” hypersensitivity delayed
Sensitized Th1 cells recognize antigens and release •pro-inflammatory cytokines.?
Type “IV” hypersensitivity Mechanism
Tuberculin skin test (TST): A small amount of the antigen, purified protein derivative (PPD) of tubercle bacilli, is injected intradermally into a person.
Interpretation of results: after 48-72 hours
This induration is due to accumulation of macrophages and lymphocytes.
(diameter !!)
Type of hypersensitivity?
Type “IV” hypersensitivity
Granuloma formation
Type of hypersensitivity?
Type “IV” hypersensitivity Examples
