Hypersensitivity reactions Flashcards
Which type of bacteria are MAC (membrane associated attack complexes) most effective?
Gram NEGATIVE bacteria
Limited peptidoglycan to fight against
Which Ig doesn’t have a hinge region, making it harder for proteases to process the antibody
IgM
Which is better at activating complement/opsonization, IgG or IgM?
IgM
But IgG is smallest antibody, so can go through vessels into tissue easier!
Because IgM is so large, it rarely enters tissue
IgM can act as a BCR when bound to B cells
Type I hypersensitivity antibody type
IgE
Type I hypersensitivity’s other name
Immediate hypersensitivity
Type II hypersensitivity’s other name
Cytotoxic hypersensitivity
Type II hypersensitivity’s antibody type
IgG, IgM
Diseases associated with Type II hypersensitivity (6)
1) Drug reactions
2) Pemphigus
3) Pemphigoid
4) IMHA
5) Transfusion reaction
6) Cryoglobulinemia
T or F: Type II hypersensitivities need complement to work
False. Many mechanisms use complement, but not complement-dependent
Mechanism of Type II hypersensitivity (5)
Antibody binds autoantigen → +/- activate complement
1) Neutrophil cytotoxicity
*Complement binds Ig → chemotaxis for neutrophil → releases proteases/ROS →cell damage
*PF
2) Opsonization + Phagocytosis
*Complement binds Ig→ chemotaxis for macrophage → eat complement and bound Ig + cell
*IMHA
3) MAC formation
4) Apoptotic response
*Complement binds Ig → chemotaxis for NK cell → release perforin, granzymes that poke holes in cell PM →lysis
5) Disruption of cell function
*NO COMPLEMENT
*Ig binds autoantigen RECEPTOR → 2 options
A) Ab binds R; Noncompetitive inhibition for R
*Myasthenia gravis
B) Ab binds R; activates R without its normal signal
*Hyperthyroidism
Type III hypersensitivity antibody type
IgG, IgM
Type III hypersensitivity’s other name
Immune-Complex mediated hypersensitivity
Diseases from Type III hypersensitivity (4)
1) SLE
2) DLE
3) Purpura hemorrhagica
4) Vasculitis
Type IV hypersensitivity antibody type
None → cell mediated
Type IV hypersensitivity’s other name
Late phase, cell mediated hypersensitivity
4 types of Type IV hypersensitivity (A-D)
A) Th1 → macrophage activation → contact dermatitis
B) Th2 → eosinophil activation → chronic allergy/asthma
C) CD8 → Cytotoxic → Contact dermatitis, EM, SJS
D) T cell → neutrophil activation
True or False: Atopic dogs typically have less IgA
True. Theory that increased IgE may be compensatory for lack of IgA
Functions of basophils (3)
1) IgE-mediated anaphylaxis
2) IgG-mediated anaphylaxis via FcgR1
3) Release PAF, which is more effective than histamine at increasing vascular permeability
PAF relative to histamine
PAF is more effective than histamine at increasing vascular permeability
PAF made by neutrophils
What can trigger cutaneous basophil hypersensitivity
Ticks, fleas, insects
*Characterized by marked basophil infiltrate and fibrin deposition
*Mediated by T cells and IgE/IgG
*Pathogenesis of IBH
Type I hypersensitivity can result 3 major mast cell product families. What are they?
Antibody cross-links to FcER1-bound IgE →FcER1 with intracellular tyrosine kinase dimerize and produce (4):
1) Phospholipase A → arachidonic acid → prostaglandins and leukotrienes
2) Protein kinase → (phospholipase C) → intranuclear → gene transcription → Cytokines
3) Protein kinase → filament formation → Granule exocytosis
*Phospholipase A for Arachidonic (A)
*Phospholipase C for Cytokine (C)
What organs normally clear immune complexes
Spleen, liver
If not→ deposited in tissue
External antigens that can trigger immune complexes (5)
1) Drug
*Dobie + sulfa drug
2) Self antigens
3) Foreign serums
*Monoclonal antibodies
4) Bacteria
5) Diet hypersensitivity
2 major forms of Type III hypersensitivity
1) Local reaction → “Arthus reaction”
*Localized necrotic vasculitis
2) Generalized reaction → “Serum sickness”
*Complement gets stuck in small vessel → activates complement → recruits neutrophil → release protease + ROS → damage to endothelial cells + vessel BMZ → leaks to surrounding tissue