Hypersensitivity Flashcards
What does cell-mediated immune response relate to?
CD4 T cells and CD8 T cells
What does humoral antibody response relate to?
B-cells
What is the classification of hypersensitivity?
Type I: IgE (allergies/basophils)
Type II: humoral antibody response to antigens on cell membrane (b-cells)
Type III: immune-complex mediated reactions (antibody-antigens)
Type IV: cell-mediated immune response (CD4 T cells and CD8 T cells)
What is a Type I hypersensitivity reaction?
IgE
a rapid reaction with an antigen with an IgE antibody that is bound to the surface of mast cells in a sensitized host
overreaction of the immune system to a normally harmless environmental allergen
etiology: previous exposure, genetic predisposition, CNS mediation
Patho: naive response stimulates IL 4, IL 5, IL 6, IL 13 production
IL 4 stimulates B cells to produce IgE antibodies
IgE antibodies attach to the Fc receptor on mast cells or basophils
this activates the mast cells and basophils to produce inflammatory response
What is a naive response?
Mature recirculating T cells that have not yet encountered their antigens are known as naive T cells. To participate in an adaptive immune response, a naive T cell must first encounter antigen, and then be induced to proliferate and differentiate into cells capable of contributing to the removal of the antigen. We will term such cells armed effector T cells because they act very rapidly when they encounter their specific antigen on other cells
What are the two responses of Type I hypersensitivity reaction?
Early Phase: rapid within 5-30 minutes and usually finished by 60 minutes
causes vasodilation, increased permeability
manifestations: rhinorrhea, edema(nasal congestions), itchy nose, bronchospasms and platelet aggregation
Late Phase: generally occurs 2-8 hours after immediate reaction; caused by infiltration of recruited neutrophils, eosinophils, basophils, monocytes, and T cells; these increased leukocytes cause inflammatory response and cause cell damage
What is the role of mast cells and basophils in Type I hypersensitivity?
mast cells are activated by: antigen cross link of IgE-Fc receptors and C3a and C5a (anaphylactoxins)
this causes: degranulation (release of mediators that produces early phase response by primary mediators)
opens mucosal intercellular junctions which allows penetration of the antigen to more numerous mast cells
release of AA (produces late phase response by secondary mediators)
basophils are the blood component to mast cells and they have cell surface IgE-Fc receptors; they also contain cytoplasmic granules which are released in IgE cross linking
What are types of Type I?
allergic rhinitis/hayfever/ashtma/food allergies/allergic drug reactions/anaphylaxis
What antibodies are involved in type II hypersensitivity?
IgG and/or IgM
What is the path of Type II?
3 mechanisms:
1: opsonization and phagocytosis: antibody binds to surface of antigen=antibody-antigen complex
* C3 opsonizes the cell surface which causes phagocytosis by macrophage
ex: transfusion reaction, autoimmune hemolytic anemia
2: inflammation and injury: antibody binds to antigen and causes antibody-antigen complex which causes C1 to activate and recruits leukocytes and causes cell injury and inflammation
ex: glomerulonephritis
3: Cellular Dysfunction: antibodies are directed against cell surface receptors and this impairs or dysregulates the function of receptor
ex: thyroid gland (graves disease) and MG (antibodies are directed to acetylcholine receptor)
What is the difference between Type II and Type III?
Antibodies attach and bind to antigens to cause cell injury and inflammation in Type II
Antibody-antigen complexes are deposited in tissues
What happens when the antibody attaches to an antigens surface?
- antibody-antigen complex is formed
- this complex always initiates C1 of complementary system=stimulates inflammatory system=stimulates neutrophils and monos/macrophges which then release enzymes and ROS to damage cell
What occurs in Type III hypersensitivity?
1: Antibody-Antigen formation
2: Immune complexes are deposited
(the small to moderate sized are more likely to be deposited and solubility, affinity of the antigen, and functional status of phagocyte system are factors as well)
3: inflammation
(complement cascade=activation of neutrophils and macrophages to phagocytose and release cytokines=vasodilation, platelet aggregation, activation of clotting cascade, and kinin system)
ex: Lupus
What occurs during Type IV hypersensitivity?
cell mediated=CD4 and CD8 T cells
1: Delayed Type
*secondary
*CD4 differentiate to Th1 and Th2
*Th1 secrete cytokines, activates mature CD8 against antigen (this causes naive response)
*cytokines (cause redness, itchy, pain) and recruit leukocytes that activate phagocytosis or release of ROS
ex: autoimmunity, transplant rejection
2: Direct T cell-Mediated Cytolysis
sensitized CD8T cells kill antigen bearing cells
*IFN(interferon which is a cytokine) are secreted which cause inflammation and injures other cells
