Download Type II hypersensitivity

Clinical Immunology:
Protection
Immune System
Reaction
Damage
Hypersensitivity
Allergy (hypersensitivity) allergy is an altered state of reactively to an
antigen or hapten, hypersensitivity means a heightened reactively.
Types of hypersensitivity:
Type Ι hypersensitivity:
IgE Mediated,Anaphylactic, Immediate (reaction with minutes )
Allergic disease
Atopic disease: In people with a hereditary predisposition to produce
(IgE) against common environmental antigen (Allergen).
Allergy
Allos
Other
Ergon
Reactivity
Molecules from outside own body ( Allergen )
Allergen: An antigen that cause allergic reaction:
Breath or take in
Food
Dender
Bee sting
Mold
Drugs and Medications
Pollens
Contact with skin
Latex
Lotions
Soaps
First exposure ͋ Sensitization ͋
Allergen
Subsequent exposure : get serious
Once again:
Type 1 Hypersensitivity:
Most allergic reaction
Genetic predisposition ( Runs in families)
Example:
Ragweed Pollen ( Allergen):
Lymph node
Antigen Presenting Cell
Dendritic cell
Macrophage
Peptides
Naïve T- Helper cell
TH‫ە‬
(Never seen antigen)
Primed T- Helper
Diferentiation
TH 2
TH 2 release cytokines such as: IL-3, IL-4,IL-5,IL-10 and others
That inhibit TH 1 cell activation
IL-4, IL13 with B- cell surface molecule CD40 induce isotype switching
of IgM bearing B-cell resulting in production of IgE.
Degranulation of Mast cells leads to release of Pro- inflammatory
mediators.
Degranulation f Esinophils leads to release of toxic substances
Pro-inflammatory mediators:
Early Phase Reaction (within minutes)
Histamine:
Bronchi-Smooth muscle contraction
-Difficulty breathing
Blood vessels-Dilation ( increase
permeability )- Edema (swelling)
Late Phase Reaction (8-12 hrs.)
Il4, IL5, IL10, Leukotrienes:
Like histamine –Smooth muscle
contraction
Attract more immune cells
(Neutrophils, Mast cells, Esinophils)
Even after allergen gone
Serotonin
Kinins
Proteases
Esinophils granules
Symptoms:
Mild Symptoms
Sever Symptoms
(Large load of allergen)
 hives (urticaria)
 eczema
 allergic rhinitis
nose
 asthma
 increase vascular permeability
 Air way constriction
can‫ ۥ‬t supply vital organs
Anaphylactic Shock
inflammation
Treatment:
 Anti-Histamine
Decrease vascular permeability
Decrease Bronchoconstriction
Anti-Histamine
Block
 Corticosteroides
Decrease inflammatory response
 Epinephrine (injection IM or IV) constrict blood vessels.
Histamine
Type II hypersensitivity:
Cytotoxic hypersensitivity
This type involves the death of cells bearing Ab attached to antigen
, Abs are of IgG & possibly IgM classes react directly with antigen
on the surface of tissue cells (SELF). Complement participate in
this reaction & promote cytolysis or cytotoxic reaction.
E.g. hemolytic reaction drug, allergies, autoimmune disease &
allograft rejection.
Drugs (eg, Penicillins) can attach to surface proteins on red blood
cells and initiate antibody formation. Such autoimmune
antibodies(IgG) then interact with the red blood cell surface result
in hemolysis.
(self)Ag-Ab Complex: Host tissue problem
Mechanisms of Type II hypersensitivity:
Cytotoxic mrchanism 1:
Complement
Small proteins
Enzymatic cascade
Fight infection
C3a, C4a, C5a are chemotactic factors attract Neutrophils
Neutrophils degranulation release enzymes :
Peroxidase
Myeloperoxidase
Proteinase
These enzymes cause RBCs lysis
Hemolytic Anemia
Cytotoxic Mechanism2:
Complement system: Membrane Attack Complex (MAC)
COOMB‫ ۥ‬S TEST:
Cytotoxic Mechanism 3:
Complement System:
C3b – Opsonization- Phagocytosis ( RBC engulfed and destroyed )
Cytotoxic Mechanism 4:
Ab- Dependent Cell Mediated Cytotoxicity (ADCC)
(Natural Killer Cell)
Non – Cytotoxic Mechanism:
eg, Myasthenia Gravis
Once again:
Type II hypersensitivity: Ab – mediated, Generally cytotoxic –
Tissue specific.
Type III hypersensitivity:
Antigen antibody complex form in the soluble or fluid phase of
tissue or in blood & then deposit on vessel walls & glomerular
membrane to interrupt normal physiological process. This lead to
complement become activated & release chemotactic factors. The
attracted leucocytes release enzymes possibly other agent that
injure local times, e.g. Arthus reaction, auto immune reaction and
glomerlonephritis.
Type IV hypersensitivity:
Delayed type reaction :- the cell mediated hypersensitivity reaction
involved antigen sensitize T-cells which respond directly or by the
release of lymphokines.
e.g. dermatitis & allergies of infections. The delayed appear of an
indurate & erythematus reaction which reaches a maximum at 24-48
hrs & is characterize histology by with mononuclear phagocytes &
lymphocytes.
The Summary of Hypersensitivity Reactions
Once again: