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Hypersensitivity reactions: is it chronic or acute pathology?
hypersensitivity rxn involve what
IgG or specific T cell
type I hypersensitivity
anaphylactic type (allergy and anaphyxasic)
type II hypersensivity
AB dependent (AB to fixed tissue antigen)
type III hypersensitivity
type IV hypersensitivty
type I - mechanism
- 1.Allergen cross-links IgE antibody to activate mast cells and Basophils
- –Initial response (5 to 30 minutes)
- 2.Release of vasoactive amines & other mediators from basophils and mast cells
- –Late-phase reaction (2 to 8 hours & lasts for days)
3.Recruitment of other inflammatory cells
4.Mucosal epithelial cell damage
true or false:
Type I hypersensitivity requires a “primed” immune system
Type I hypersensitivity is quality and location dependent
activating mast cell
C3a and C5a
IgE on mastcell
Initial phase - type I
One of the key immediate mediators is histamine. It causes a rapid increase in vascular permeability as well as contraction of smooth muscle.
Histamine ↑ vascular permeability vasodilation bronchoconstriction mucus production
key mediator in initial phase of Type I
beside histamine, what else is produce in initial phase?
- protease (tryptase)
- chemotactic factors (eosinophil and neutrophil)
Late phase - type I produces what molecule
: TNf a, IL-1, IL-4, IL-5, IL-6 --> recruit and activate many types inflammatory cells
- C4&D4 - asoconstriction
- B4 - chemotactic: Eosinophil, neutrophil, monocytes & leukocyte adhesion
Protaglandin D2: vasodilation, mucous secretion
- Platelet-activating factor
- platelet aggregation
- 100x > histamine (inc vascular permeability, vasodilation)
- chemotactic for eosinophil & neutrophils
which phase is the major cause of symptoms in Type I hypersensitivity disorders?
timeline for type I hypersensitivity (early and late phase)
- early phase: minutes
- Late phase: hours-days
classic example of type I IgE mediated hypersensitivity.
predisposition to develop localized immediate hypersensitivity reactions to a variety of inhaled and ingested allergens
Atopic individuals tend to have higher serum IgE levels, more IL-4 producing TH2 cells, compared with the general population.
family history is common
2nd exposure of antigen to atopic asthma
- releases mediators that open mucosal intercellular junctions > more antigen reaches mast cells
- --> bronchoconstriction, edema, mucus secretion
Late phase response: inflammatory cell recruited including eosinophils (amplify and sustain inflammatory response)
airway remodeling from atopic asthma
-Thickening of the basement membrane of the bronchial epithelium
-Edema and an inflammatory infiltrate in the bronchial walls, with a prominence of eosinophils and mast cells
An increase in the size of the submucosal glands
Hypertrophy of the bronchial muscle walls
•GI tract musculature over activity
anaphylactic shock --> systemic vasodilation
testing for systemic type I hypersensitivity
injection and test and wheal and flare
atopic asthma - clinical course
- Asthmatic attack lasts up to several hours and causes recurrent episodes
- Chest tightness, breathlessness, wheezing
- Cough without sputum
- Difficulty exhaling (air is trapped distal to bronchi)
- Asthma attack due to
- Intermittent and reversible airway obstruction
Chronic bronchial inflammation with eosinophils
Bronchial smooth muscle cell hypertrophy and hyper-reactivity (bronchoconstriction)
type II HS - diseases
- -Normal cell surface molecule
- Goodpasture’s Disease – anti-glomerular
- basement membrane protein
- Graves Disease (hyperthroidism): Ab
- mediated TSH stimulation
- -Adsorbed exogenous antigens (Drug or metabolite)
- Hemolytic anemia or thrombocytopenia
- •is an autoimmune disease in which kidney and lung injury is caused by circulating
- autoantibodies against the basement membrane type IV collagen.
•Teens-20’s; males mostly
- •Initiate inflammatory destruction of the basement membrane in renal glomeruli and
- pulmonary alveoli > proliferative and rapidly progressive glomerulonephritis and necrotizing hemorrhagic interstitial pneumonia
Get nephritis and lung hemorrhage
Mechanism for Antibody Mediated Injury
Complement Dependent reactions
Antibody-Mediated Cellular Dysfunction
Complement-Dependent Reactions - type 2 HS
–Direct cell lysis
–Opsonization and Phagocytosis
- Ab binding to Fc receptors on macrophages
- as well as complement breakdown production induce inflammation.
Complement-Dependent Reactions - type 2 HS
- •Transfusion reactions
- –Blood grp Ags
- •Erytroblastosis fetalis (Immune Hydrops)
- –Rh incompatibility
- –ABO incompatibility
•Autoimmune hemolytic anemia, autoimmune thrombocytopenic purpura
- produced against self-blood cells
- •Drug reactions
- –Penicillin adsorbed to cell surface
- •Pemphigus vularis
- –Abs against desmosomal
- proteins that lead to disruption of epidermal intercellular junctions
- •a blistering disorder caused by IgG antibodies directed against epidermal
- cadherin (protein in intercellular junctions of epidermal cells)
•Pemphigus vulgaris is most common type. Lesions are first seen in oral and genital mucosa.
Superficial blisters that rupture easily
- Ab disrupts intercellular adhesions,
- leading to inflammation, leading to blisters.
•Similar to Pemphigus vulgaris but IgG antibodies disrupt the basal cell-basement membrane attachments (hemidesmosomes).
•Blisters form that do not rupture easily.
•Oral involvement is present in 1/3 of patients.
•More common in elderly.
Antibody-mediated cellular dysfunction
- Myasthenia gravis
- grave disease
Anti-receptor antibodies disturb the normal function of receptors.