Type1Hpersensitivity Flashcards
Roles of IgG in helminth immunity
Roles of IgG in helminth immunity IgG: binds (coats) the worm or its ova → activates complement → C3a and C5a attracts neutrophils → neutrophils arrive and seize opsonized worm with their IgG and C3 receptors → Neutrophils lack helminthocidal mechanism → IgE to the rescue!
Roles of IgE in helminth immunity
worms shed antigens → diffuse to nearby mast cell → FCeR of mast cells become loaded with anti-helminth IgE → worms antigen cross links the IgE → mast cells degranulate → release Histamine → cause gut smooth muscle contraction → peristalsis expels worms
Roles of M2 in helminth immunity
Th2 finds helminth antigens presented by APC → secretes IL-4, IL-5, IL-13 → attracts M2 macrophages → heal damage and wall off M1-resistant helminthes
Roles of Eosinophils in helminth immunity
have Fc receptor for IgG (which Is coating worm) → binds to opsonized worm → release granules containing Major Basic Protein (MBP) → toxic to helminths
- Eosinophils are also attracted by Th2
What does eosiniphilia in the blood/sputum a sign of?
sign of parasitic disease or severe Type I immunopathology
What are attracted by Th2 when it comes to helmith immunity?
M2 macrophages (by way of IL-4, 5 and 13)
Eosinophils
Atopic
Atopy, atopic disease, and allergy are all synonymous and means “prone to develop any of the range of allergic syndromes” - Not helpful I know.
Immediate hypersensitivity
Person has already made IgE
Allergy
an atypical immune response to environmental antigens, eventually becoming characterized by increased reactivity of the end-organs to inflammatory mediators and irritants.
○ hypersensitivity disorder of the immune system.
○ Roughly same thing as atopy
approximate incidence of atopic diseases in the general population, and in individuals with allergic parents.
○ ~20% of all people have it
35% ↑er risk with 1 allergic parent
65% ↑er risk with 2 allergic parents
mechanism of IgE-mediated hypersensitivity: Immediate reaction
- IgE binds strongly to FCeR receptors on surface of mast cells (basophil IgE receptor) →
2. When 2 adjacent IgE molecules bind to mast cells and become cross-linked by allergen→
3. Mast cells release granules (containing histamine, heparin, enzymes, and TNF) → rapid action
mechanism of IgE-mediated hypersensitivity: Late-Phase reaction
- Activated Mast cell also initates series of enzymatic steps:
a. Phospholipase A (PLA2) cleaves arachidonic acid (aa) from membrane phospholipid → aa is converted via COX-pathway to prostaglandins or via Lipoxygenase to leukotrienes →prostaglandins and leukotrienes Initate inflammation and bronchoconstriction
i. Prostaglandins and leukotrienes that are initiated by mast cells are activated compounds. Together are called “eosinophil chemotactic factor of anaphylaxis” (ECF-A) → Really really good at attracting eosinophils in large numbers - Mast cells release cytokines also I guess . . . (he threw that little factoid in as an after thought)
How to treat:
IgE-mediated hypersensitivity (Immediate reaction)
use antihistamines (receptor antagonists). Done son!
How to treat:
IgE-mediated hypersensitivity (Late-Phase reaction)
. To treat the late-phase rxn, use B-adrenergic agonists
- can’t use antihistamines since it depends on prostaglandins, leuktotrienes and cytokines. Darn.
What does Histamine do?
Histamine results in:
local/systemic vasodilation,
increased permeability,
gut and bronchial smooth muscle contraction