Hypersensitivity Flashcards
Type I Hypersensitivity
Immediate, mediated by IgE via Mast Cell effectors:
- Histamine (vasodilator) proteases, PGs, LTs, cytokines, - PG’s cause endothelial dilation and LKs cause vascular constriction at post cap venules, causes edema
Triggered by environmental Ags, increases with more atopy (more likely to develop allergic reactions)
IgE binds FcERI (CD23) on Mast cells
Type I Hypersensitivity Early v. Late Phase
Immediate vascular and smooth muscle reaction to allergen develops in minutes
Late phase occurs 2-24 hours later
-inflammatory infiltrate rich in eosinophils, neutrophils, T cells
Allergen Specific Immunotherapy (Allergen-SIT)
Administration of increasing doses of allergen to induce:
- peripheral T cell tolerance*** (make Treg cells)
- decrease IgE histamine release
- modulate mast cell and basophil activation thresholds
Type II Hypersensitivity
Ab mediated (IgM, IgG activate complement system, activate leukocytes)
Opsonization/phag of cells
Type II Effector Mechanisms
Abs opsonize cells, activate complement, phag via FcR or CR1 for C3b
C3a and C5a recruit leukocytes
Abs specific for cell Rcs could stimulate activity of TSH (graves-hyperthyroid) or inhibit Ach binding to AchR (myasthenia gravis)
Type III Hypersensitivity
Ab-Ag complexed deposited in vessels, induce vascular inflammation, ischemic damages
Activate classical complement and recruit leukocytes
I.E. Lupus, serum sickness, Arthus reaction, polyarteritis nodoas, post strep glomerulonephritis
Arthus Reaction
Subcutaneous admin of protein Ag to previously immunized animal
Formation of Ag complexes at site of admin, local vasculitis compared to systemic serum reaction
Type IV Hypersensitivity
T CELL MEDIATED
Major triggers are autoimmunity, persistent environmental Ags, microbial Ags (M. Tuberculosis)
Mac activation/inflammation from cytokines from Th1, Th17, CTLs
Examples of Type IV Hypersensitivity
MS, Type 1 Diabetes, Crohn’s, Contact sensitive from poison ivy, chronic infections
DTH Reaction
Cytokine mediate inflammatory reaction from mainly CD4+ cells
Mainly from poison ivy, TB, tetanus, PPD (myco tuberc.)
Could result in allergic contact dermatitis (i.e. nickel)
How is a TB Granuloma Formed
Powerful Th1 inducer, surround by immune cells
Th1 and Macrophages activated by IFN-y, produce TNF
TNF and IFN-y further stimulate macrophages
Fibroblasts cover the edges, by the time CTLs get there to get rid of TB, the granuloma is too big
Systemic Lupus Erythematosus
Type III Hyper.
Rashes, arthritis, glomerulonephritis
Anti-DNA Abs (anti nuclear IgG)
Rheumatoid Arthritis (RA)
Type II/III hyper.
Th1, Th17, activated B cells and plasma cells, Macrophages
Circulating IgG/IgM that react with Fc of own IgG molecules
Auto Abs called rheumatoid factors
