Class #9 (part 2) - Hypersensitivity Flashcards
Four types?
What is hypersensitivity?
Type I - Immediate/allergy
Type 2 - Antibody-mediated
Type 3 - Immune complex-mediated
Type 4 - Cell-mediated
Def: Reaction by immune system that damages the body instead of protecting it
Type I - Immediate/allergy mechanism?
Activation of Th2 CD4+ by envir. antigens presented by B-cells -> Th2 produce IL-4 -> B-cell class switching -> Prod. of IgE by B cell -> IgE bind to Fc Epsilom receptors on the surface of mast cells -> Antigens bind to now attached IgE and Activate Mast cell to release Histamine/other mediators
What IL induce mucous production?
IL-13
Late phase of type1 mediated by?
Eosinophils
Characteristics of bronchial asthma?
a) More mucous producing cells in the epithelium = Goblets cells
b) Hypertrophy of smooth musc.
c) Fibrosis around alveoli
Local vs systemic type I hyper.
Local: Antigens confined (Eg. skin, git)
Systemic = Anaphylaxis
Hygiene hypothesis to explain type 1?
Phenotype Th1 = NO allergies. Factors favoring: Early exposure, rural envir., presence older siblings
Phenotype Th2 = Allergies. Factors favoring: Widespread use ATB, only child, urban envir.
At birth Th2, but can turn into Th1.
Type 2 - Antibody-mediated general mechanism of action?
Are caused by antibodies that bind to fixed tissue or cell surface antigens, promoting phagocytosis and destruction of the coated cells or triggering pathologic inflammation in tissues.
Type 2 usually mediated by Ig…?
IgG
Type 2, 3 specific mechanism of actions?
1) Phagocytosis: IgG bind to cell/activate complement and phagocytes eat the target cell
2) Inflammation: C5a and C3a lead to recruiment of neutro and causing inflammation.
3) Blocking receptor function: (Eg. Graves disease, Ig bind to TSH receptor stimulating thyroid cell to produce T4/T3, resulting in hyperthyroidism.)
Type 2 Eg/
1) Graves disease, Ig bind to TSH receptor stimulating thyroid cell to produce T4/T3, resulting in hyperthyroidism.
2) Myasthenia gravis: Ig bind to Ach receptor blocking Ach stimulation of musc.
3) New born hemolytic anemia: mother Rh-/Baby Rh+, first exposure mother develop anti-Rh Ig. 2nd pregancy, Ig bind to RBC of baby and initiate immune reaction.
Type 3 mechanism of action?
IgG bind to soluble antigens creating a complex that will deposit itself on basement membrane of tissues -> Activating complement cascade
4 classic Sx of reaction to foreign serum (type 3)?
Fever, Vasculitis, Arthritis, nephritis
Type 4 CD4+ mechanism of action? + can also create? +Eg
Delayed-type hypersensitivity (24hours+): Naive T-cell differentiate into either Th1 or Th17 after presentation of antigens by dendritic cell -> upon 2nd expose the memory T-cell Th1 will release IFNgamma (Th17 - IL17) -> activating macrophage -> they release proinflammatory mediators -> causing tissue damage
Can also create granulomas.
Eg: Poison Ivy -> Urushiol (hapten)
Type 4 CD8+ mechanism of action? + Eg
CD8+ recognize antigens on MHC class 1 as non-self and destroy the cell. Eg: DM type1 => Attack beta-cell in pancreas (secrete insulin), leave alone alpha cell (glucagon)
