Shnyra- Hypersensitivity Flashcards
(44 cards)
What mediates Type I hypersensitivity responses?
IgE. They result from the actions of mediators secreted by mast cells
What mediates Type II hypersensitivity responses?
IgG & IgM that bind tissues Ags & cause complement-dependent tissue injury/disease
What mediates Type III hypersensitivity responses?
Circulating Ag-Ab complexes which deposit in vessel walls & cause complement dependent injury in vessel walls
What mediates Type IV hypersensitivity responses?
T cells & results from inflammation caused by cytokines produced by CD4+ Th1 cells, Th17 cells, and macrophage or killing host cells by CD8+ CTLs
Define atopy
A genetic tendency to develop allergic diseases/allergic rxns
What do the effects of histamine, prostaglandins & leukotrienes combined induce?
Increases in BP & permeability
What causes edema?
Increased movement of fluid from the intravascular to the interstitial space
In the mechanism of edema, how are leukotrienes and histamine different?
Leuko-drain larger venules (vasoconstriction)
Histamine- post cap venules (vasodilation)
Before clinical presentation, what is occurring in the process of immediate hypersensitivity?
Activation of Th2 cells by first exposure to allergens & generation of plasma cells which produce IgE, IgE bind to FceR1 receptors on mast cells
What are late phase Type I hypersensitivity rxns characterized by?
Inflammatory infiltrate rich in eosinophils, neutrophils, & T cells
What are the 4 purposes of Allergen Specific Immunotherapy?
- induce peripheral T cell tolerance
- Increase thresholds for mast cell & basophil activation by allergens
- to decrease IgE-mediated histamine release by mast cells
- to generate allergen-specific inducible FOXP3+ CD4+ CD25+ Treg cells
In terms of allergen desensitization, define immune deviation
Repeated exposure to desensitizing allergen induces a shift from Th2 to Th1 CD4 cells that results in the generation of cytokines (IFN-y) which inhibit IgE production
Explain Type II Hypersensitivity
IgG can opsonize cells that leads to phagocytosis of the cells through FcyR or CR1 receptors. Neutros and macros that are activated in this manner release their inflammatory mediators (ROS & lysosomal enzymes damage the adjacent tissues & cause inflammation)
IgM and IgG can act. classical pathway which produces C5a and C3a which promote leukocyte recruitment & inflammation
What do Ab-dependent effector mechanisms of Type II Hypersensitivity require?
Immune cells expressing Fcy receptor type III (FcyRIII) on their surface & target cells coated with Ab recognizing ags on the cell surface
NK cells express high levels of FcyRIII & are regarded as the key players in this process
What is myasthenia graves?
Inhibiting of the binding of acetylcholine neurotransmitter to the ACh receptor that causes autoimmunity
Define immune-complex anemias
Abs form immune complexes with a drug. the ICs can bind to the erythrocyte surface via CR1. Complement is activated on RBC surface which causes hemolysis
Define autoimmune anemias
Drug induces anti-drug Abs that cross react with an Rh Ag on RBCs. Ab binding to Rh Ag activates phagocytosis & complement. Treatment may require immunosuppression or removal of ICs by plasmapheresis
What is serum sickness (Type III hypersensitivity)?
Can be induced by IV administration of a protein Ag to a previously immunized patient that leads to formation of IC and systemic vasculitis
What is arthus rxn (Type III hypersensitivity)?
Induced by subcutaneous administration of a protein Ag to a previously immunized animal. Ag causes local formation of ICs at the site of AG injection that leads to local vasculitis (compare to the systemic vasculitis in serum sickness)
What 3 things trigger a Type IV hypersensitivity reaction?
Autoimmunity
Persistent responses to environmental Ags
Microbial Ags
How long does it take a Type IV hypersensitivity rxn to occur & what is it mediated by?
24-48 hours & it is mediated by Ag-activated CD4+ T cells, CD8+ T cells, and macrophages which release mediators
What is central tolerance?
Induced by immature self-reactive lymphocytes in the primary lymphoid organs. Ensures that mature lymphocytes are not reactive to self Ags
What is peripheral tolerance?
Induced in mature self-reactive lymphocytes in peripheral sites. Prevents activation of these potentially dangerous lymphocytes in the tissues
In terms of central tolerance, what is positive selection?
Thymocytes that bind self-Ags below a certain threshold are positively selected & are allowed to migrate into the periphery as mature T cells
