Type1Hpersensitivity Flashcards

1
Q

Roles of IgG in helminth immunity

A

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!

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2
Q

Roles of IgE in helminth immunity

A

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

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3
Q

Roles of M2 in helminth immunity

A

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

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4
Q

Roles of Eosinophils in helminth immunity

A

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
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5
Q

What does eosiniphilia in the blood/sputum a sign of?

A

sign of parasitic disease or severe Type I immunopathology

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6
Q

What are attracted by Th2 when it comes to helmith immunity?

A

M2 macrophages (by way of IL-4, 5 and 13)

Eosinophils

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7
Q

Atopic

A

Atopy, atopic disease, and allergy are all synonymous and means “prone to develop any of the range of allergic syndromes” - Not helpful I know.

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8
Q

Immediate hypersensitivity

A

Person has already made IgE

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9
Q

Allergy

A

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

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10
Q

approximate incidence of atopic diseases in the general population, and in individuals with allergic parents.

A

○ ~20% of all people have it
35% ↑er risk with 1 allergic parent 

65% ↑er risk with 2 allergic parents

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11
Q

mechanism of IgE-mediated hypersensitivity: 
Immediate reaction

A
  1. 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
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12
Q

mechanism of IgE-mediated hypersensitivity: 
Late-Phase reaction

A
  1. 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
  2. Mast cells release cytokines also I guess . . . (he threw that little factoid in as an after thought)
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13
Q

How to treat:


IgE-mediated hypersensitivity (Immediate reaction)

A

use antihistamines (receptor antagonists). Done son!

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14
Q

How to treat:


IgE-mediated hypersensitivity (Late-Phase reaction)

A

. To treat the late-phase rxn, use B-adrenergic agonists

- can’t use antihistamines since it depends on prostaglandins, leuktotrienes and cytokines. Darn.

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15
Q

What does Histamine do?

A

Histamine results in: 

local/systemic vasodilation,

increased permeability, 

gut and bronchial smooth muscle contraction

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16
Q

Why do we lump atopic diseases together?

A

Cross-reactions are common in atopic disease.

For example, a person with T cellmediated contact dermatitis to latex (gloves, catheters, condoms) may have symptoms of IgE-mediated oral allergy to avocados, bananas, or chestnuts, all of which contain a cross-reactive antigen.

17
Q

Asthma definition

A

reversible bronchoconstrictive disease with progressive inflammation leading to fibrosis.

18
Q

reasons for using glucocorticoids in asthma treatment.

A

○ Risky w/ side effects w/ chronic use, but good in that they:

- Inhibit production of arachadonic acid from phospholipids → block PG and LT synthesis (late phase reaction)

- Induce apoptosis in eosinophils (remember Late-phase reactions attract a ton of them)