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Hypersensitivity (Part 2), Local reactions may occur when antigens are -…
Hypersensitivity (Part 2)
Type III hypersensitivity
Immune complex-mediated (IgG)- large amount of Ag and Ab form complexes in blood
Immune complex disease
Cons: If not elmiinated, can deposit in capillaries/ joints
Frustrated phagocytes
If neutrophils and macrophages unable to phagocytize immune complexes
They degranulate in area of immune complex deposition and trigger inflammation
Mechanism
PMNs and macrophages bind to immune complexes via FcR and phagocytize the complex
Can trigger inflammation via C' activation
C3a, C4a, C5a and "frustrated phagocyte"
Mechanism
IgG/igM antibodies bind with soluble antigen from medications or animal venom
Immune complex forms and binds with C1 to produce C5a and c3b
Neutrophils bind to the immune complex and C3b attached to the tissue
Granules with Oxygen Reactive Species released and cell destruction leads to tissue damage
Type of Type III Sensitivity Reactions
Localized
eg: Arthus reactions
Inhaled (eg: Farmer's Lung & Pigeon Breeder Disease)
Injected (eg: Tetanus vaccination)
Ingested (eg: Celiac disease)
Systemic
Ex: Serum sickness
in Raynaud phenomenon: cryoglobulins blocking capillary
cause Cyanosis (from O2 deprivation)
Symptom: pallor & numbness
from large amounts of Ag : injection of foreign serum
usually transient immune complex disease with removal of Ag source
Ex: Systemic Lupus Erythematosus (SLE)
Immune complexes attach to
Endothelium of blood vessels
symptom: vasculitis
Glomerular capillaries (Kidney)
symptom: acute glomerulonephritis
Rheumatoid Arthritis (AR)
General characteristics of phatophysiology of Delayed-typed hypersensitivity (DTH)
Stages of Type IV DTH
Sensitization stage
Dendiritic cells generate memory Th1 cells against STH antigens
Th1 cells can activate macrophages and trigger inflammatory
Effector stage
Secondary contact yields
Th1 cells are activated
produce cytokines
eg: IFN-g, TNF-a & TNF-b
tissue destruction
inflammation
IL-2
activates T cells & CTLs
Chemokines
macrophage recruitment
IL-3 & GM-CSF
increased monocyte/macrophage
Effector stage
due to secondary exposure to antigen
activation of clotting cascades & tissue repair form tissue damage
fluid filled can form lesion
inflammed area becomes red
continued exposure can cause chronic inflammation
cause granuloma formation
Phases of DTH response
Sensitization phase
Examples of DTH
Contact dermatitis
response to poison oak (classic type IV)
small molecules acts as haptens & complexes with skin proteins
take up by APCs & presented to Th1 cells
get sensitization
During secondary exposure: Th1 memory cells become activated to cause DTH
Mechanism
poison oak releases pentadecacatechol
sensitized TDTH self-protein takes up the molecule
molecule was taken up & presented by APC (Langerhans cell) to Th1 cells
Th1 cell releases IFN-y, MIF & MCF
uptake of MCF by macrophage (tissue)
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uptake of MIF by monocyte (bloodstream)
Intracellular pathogens & contact antigens that induced DTH
Granula formation (by Chronic inflammation)
Treatment of DTH
Type IV hypersensitivity (Delayed type hypersensitivity)
Mechanism
involves Th1 cells and macrophages
Response from
Th1 cells release cytokines to activate macrophages cause
inflammation
tissue damage
Continued macrophage activation cause
scarring
tissue lesions
granula formation
is relative: DTH response arise 24-72 hours after exposure rather than within minutes
cell-mediated/delayed type hypersensitivity
a hypersensitive responsed mediated by sensitized TDTH cells, which release various cytokines & chemokines
generally occurs 2-3 days after TDTH cells interact with antigen
an important part of host defense against intracellular parasites & bacteria
Local reactions may occur when antigens are
