Hypersensitivity Reactions Flashcards Preview

Block 2 Immunology > Hypersensitivity Reactions > Flashcards

Flashcards in Hypersensitivity Reactions Deck (9)
Loading flashcards...

Are people born with an effector response to allergens? Why or why not?

- No, there must be a first exposure to the allergen in which the primary immune response is generated, but no symptoms of hypersensitivity are experienced 

- After this first exposure, subsequent exposures elicit hypersensitivity response and its symptoms 



Describe the 7 features of inhaled allergens that may promote the priming of TH2 cells that drive IgE responses, and lead to immediate hypersensitivity.

- Molecular type: must be proteins b/c must be T-dependent antigens. T-helper cell response is needed for activation of B cells, and class switching to IgE

- Function: very often proteases (typical mast cell effector function is to expel parasites, and they produce abundant enzymes to allow them to remodel tissue, move around) 

- Low dose: low antigen dose favors differentiation of TH0 cells into TH2 effector type 

- Low molecular weight: if protein is small, it can diffuse out of dust particle that delivered in into respiratory tract

High solubility: the more soluble, the more effectively the allergen will elute out of its dust particle

Highly stable: must be stable to survive when part of desiccated (dehydrated) particle

- Contains peptide that binds MHC II: required for any T-dependent antigen


What are Type IV hypersensitivity reactions?

- Delayed type: Mediated by T cells (either CD4+ or CD8+ T cells)

- It takes 24-72 hours for T cells to initiate symptomatic inflammatory responses


- Immune reactant: 1) TH1, 2) TH2, 3) CTL

- Antigen:

1 & 2. Soluble antigen 

3. Cell-associated antigen  

- Effector mechanisms: 

1. Macro activation 

2. Eosinophil activation 

3. Cytotoxicity 

- Examples: 

1. Contact dermatitis, tuberculin rxn 

2.  Chronic asthma, chronic allergic rhinitis

3.  Contact dermatitis 


What are Type I hypersensitivity reactions?

- Immediate-type hypersensitivity reactions: initiated by mast cell degranulation, mediated by crosslinking of IgE bound to high affinity IgE receptors of mast cells 

- Occur within minutes following exposure to antigen


- Immune reactant: IgE 

- Antigen: soluble 

- Effector mechanism: mast-cell activation 

- Examples: allergic rhinitis, asthma, systemic anaphylaxis


What are Type II hypersensitivity reactions?

- Altered self hypersensitivity reactions: initiated by allergen-specific IgG antibodies, and the inflammatory response is mediated by the complement cascades, phagocytes and NK cells

- Take longer to develop than Type I reactions: 4-12 hours


- Immune reactant: IgG

- Antigen: 

1. Cell- or matrix-associated Ag 

2. Cell-surface receptor

- Effector mechanism: 

1. Complement, FcR+ cells (phagocytes, NK)

2. Ab alters signaling 

- Examples: 

1. Some drug allergies, e.g., penicillin 

2. Chronic urticaria (Ab to FalphaRIalpha) 


What molecular mechanism prompts mast cell degranulation?

- Crosslinking of the IgE Abs bound to high affinity IgE receptors on mast cell surface


What are the enzyme, toxic mediator, and chemokine effector molecules of mast cells?

- Enzymes: tryptase, chymase, cathepsin G, and carboxypeptidase -> remodeling of CT matrix 

Toxic mediator: histamine, heparin -> toxic to parasites, increase vascular permeability, cause smooth muscle contraction

- Chemokine: CCL3 -> chemotactic for monocytes, macrophages, and neutrophils 


What are the cytokine and lipid mediator effector molecules of mast cells?

- Cytokines: 

1. TNF-alpha: promotes inflammation, stimulates cytokine production by many cell types, and activates endothelium 

2. IL-4, IL-13: stimulate/amplify TH2-cell response 

3. IL-3, IL-5, GM-CSF: promote eosinophil production and activation

- Lipid mediators:

1. Leukotrienes C4, D4, and E4: cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion 

2. Platelet activating factor: chemotactic for leukocytes, amplifies production of lipid mediators, activates neutrophils, eosinophils, and platelets


What are Type III hypersensitivity reactions?

- Immune complex hypersensitivies: result of immune complex deposition and ensuing inflammatory responses as phagocytes encounter these immune complexes deposited in the host tissues

- Altered-self hypersensitivities (type II) often become immune complex hypersensitivities.


- Immune reactant: IgG

- Antigen: soluble antigen 

- Effector mechanisms: complement phagocytes 

- Examples: serum sickness, Arthus reaction