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Immuno > Unit 4 Lec 5 > Flashcards

Unit 4 Lec 5 Flashcards

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0
Q

What is an unique feature of type I hypersensitivity?

A

Immediate response (seconds-minutes)

  • IgE
  • Cells with granules: Mast Cells, Basophils, Eosinophils
  • Very common
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1
Q

What is type I hypersensitivity?

A

Immediate hypersensitivity
IgE-mediated hypersensitivity
- Allergic disease

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2
Q

What are allergens?

A

Immune response to nonmicrobial environmental antigens

  • Allergic or Atopic disorders
  • Most common 20%
  • 2x increase prevalence in the past 15 years
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3
Q

What has a strong genetic predisposition?

A

Allergic response
- If both parents are allergic child has 40-60% chance of developing allergy

  • If neither parent has allergies then child has about a 10 percent chance of developing allergy
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4
Q

What are allergens?

A

Proteins (chemicals bound to proteins to which the atopic individual is chronically exposed

  • Proteins in pollen, house dust mites, animal dander, foods
  • Chemicals (i.e. penicillin)
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5
Q

What are some common features of allergens?

A

Glycosylated, low medium molecular weight highly soluble in body fluids
- Atopic individuals produce high levels of IgE in response to environmental allergens

  • Highly soluble allows them to go through mucous membranes
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6
Q

Why do we get allergic disease?

A

Genetic susceptibility of Environment

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7
Q

What is the hygiene hypothesis?

A

Postulate that exposure to some infections and common environemntal microorganisms in infancy and childhood drives the immune system towards a general state of non-atopy

  • But children with a genetic susceptibility to atopy and who live in an environment with low exposure to infectious disease are though to be more susceptible to the development of atopic/allergic disease
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8
Q

What is the hallmark of allergic diseases?

A

Activation of Th2 cells and production of IgE

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9
Q

What is the typical sequence of immediate hypersensitivity reactions?

A

Exposure to antigen– activate Th2 ells and B cells— production of IgE antibody– binding of antibody to Fc receptor of mast cells– triggering the mast cells by re exposure to the antigen resulting in release of mediators from mast cells and subsequent

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10
Q

What is essential to the production of IgE?

A

Th2 cells through secretion of IL-4, IL-13 which stimulate B cells to undergo heavy chain isotype switching and produce IgE.

IL-5 activates eosinophils,

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11
Q

What are the clinical manifestations of immediate hypersensitivity?

A

Vascular and smooth muscle reaction developing rapidly after repeated exposure to the allergen

Delayed inflammatory reation (

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12
Q

What needs to occur to activate the release of granules?

A

Crosslinking of IgE on mast cells

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13
Q

What are mast cells activated by?

A

Cross-linking of FceRI molecules’takes only seconds to go from cross linking to release of mast cell granules

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14
Q

What are the effector cells of the immediate hypersensitivity reaction?

A

Mast cells, basophils, eosinophils
- Function are mediated by soluble molecules released upon activation of these cells
-

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15
Q

What are the 3 common findings for 3 share common features?

A

Cytoplasmic granules whose contents are the major mediators of allergic reactions
- Lipid mediators and cytokines that induce inflammation

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16
Q

What is major biogenic amine mediator in mast cells?

A

Histamine

- H1, H2, H3 blocked anti-histamine medications

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17
Q

What is responsible for wheal and flare?

A

Histamine

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18
Q

What are some lipid mediators of mast cell?

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A

Arachidonic acid goes to cyclo oxygenase lipooxygenase

Membrane phosopholipids are hydrolyzed by phospholipase A2 (PLA2) to generate Arachidonic Acid, metabolized by the cyclooxygenase lipoxygenase pathways to produce lipid mediators

19
Q

What is stored in the granules of mast cells?

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A

Mast cells and basophils mediators hold cytokines and lipid mediators that are newly synthesized on cell activation

20
Q

What do biogenic amines and lipid mediators induce?

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A

Vascular leakage, bronchoconstriction, and intestinal hypermotility (all components of the immediate response)

21
Q

What do cytokines and lipid mediators contribute to?

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A

Inflammation (late-phase) reaction

22
Q

What can enzymes of the activated mast cells contribute to?

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A

Contribute to tissue damage

23
Q

What do activated eosinophils release?

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A

Preformed cationic proteins as well as enzymes that are toxic to parasites and host cells

24
How do immediate hypersensitivity reactions manifest?
Manifest in different ways Depending on tissue affected (includes rashes, sinus congestion, bronchial constriction, abdominal pain, diarrhea, and systemic shock
25
What is the most extreme form of immediate hypersensitivity?
Anaphylaxis (mast-cell) derived mediators
26
How do CD4 T cells play a role in immediate hypersensitivity?
T cell independent antigens (polysaccharides) cannot eliciity reactions unless become attached to proteins - Plays a role as some drugs (penicillin) react chemically with amino acid residues in self proteins to form hapten-carrier conjugates--- stimulate Th2 and IgE production
27
What does the regulation of IgE synthesis depend on?
Propensity of an individual to mount a Th2 response | - Influenced by genetic factors, nature of allergen, and history of allergen exposure
28
What is IgE responsible for?
For sensitizing mast cells and provides recognition of antigen for immedediate hypersensitivyt reactions - Binds high affinity IgE receptor FceRI on mast cells and basophils even in ABSENCE OF BOUND ALLERGEN - Affinity higher than any other Fc receptor for its antibody ligand
29
What does Th2 cells produce that activate components of hypersensitivity?
IL-4, IL-13 to activate B cells IL-5 to activate Eosinophils (LATE PHASE)
30
What is the immediate reaction to allergen?
Wheal and Flare - Red (locally dilated blood vessels) - Swells as a result of leaky endothelial cells (venules)= WHEAL - BLood vessels at margins of wheal dilate and become engorged= FLARE
31
What happens in Late Phase Reactions?
Accumulation of inflammatory WBCs - Primary eosinophils, Th2 cells, and basophils, neutrophils can be present - Clinically in patients with long term exposure to allergens - Chronic allergic inflammation ensue - Primarily mediated by Th2 cells - Long term serious illness such as asthma
32
What does allergen administration determine in the resulting type of IgE mediated allergic reaction
Route and dose determine the type of IgE mediated alergic reaction
33
What are mast cells associated with?
Associated with vascularized connective tissue called connnective tissue mast cells Associated with submucosal layers of the gut and respiratory tract are called mucosal mast cells
34
What occurs in anaphylaxis?
Commonly caused by medicaitons Symptoms from Urticaria to potentially fatal ANAPHYLACTIC SHOCK - Anaphylaxis is a systemic immediate hypersensitivity reaction from the systemic presence of an allergen
35
What happens in anaphylatic shock?
Massive release of histamine to become widespread and increase vascular permability decreases blood pressure to send person into SHOCK - Rapidly fatal if not treated - Epinephrine is life saving because reverses bronchoconstrictive and vasodilatory effects of mast cell mediators
36
What is allergic asthma?
IgE mediated reaction to allergen exposure in lower respiratory tract - Same allergens that cause allergic rhinitis/conjunctivitis Shortness of breath, wheezing, cough (bronchial constriction) - Asthmatic attacks can be life threatening
37
What happens to repeated immediate hypersensitivity reactions effect on the lungs?
Intermittent and reversible airway obstruction Bronchial smooth muscle hypertrophy and hyperreactivity - eventually develop fibrosis
38
What happens in chronic airway inflammation?
Mediators released by Th2, eosinophils, neutrophils Airway tissue remodeling Smooth muscle hypertrophy, thickening of airways fibrosis Airways become hyperactive and other factors can trigger asthma attacks
39
How to treat allergic disease?
Trigger avoidance Inhibition of effector pathway - Treatment is palliative, rather than curative - Frequently taken lifelong Desensitization
40
What would be a way to inhibit the effector mechanism?
Inhibit IgE (Omalizumab) Block IL-5, IL-4, IL-13 (under trials
41
What blocks histamines?
THe use of antihistamines i.e. H1 receptor antagonists | - There are sedating and non sedating
42
How do you block lipid mediators?
NSAIDS against cyclo-oxygenase Zileuton aginst lipo-oxygenase Montelukast against LT B4, C4, D4, E4
43
What treats inflammaiton?
Corticosteroids (systemic, inhaled, nasal) Bronchodilators (beta agonists0 Epinephrine (acutely) (to treat acute vasodilation)
44
What is desensitization immunotherapy?
Restore tolerance to the allergen by reducing its tendency to induce IgE production Injections of escalating doses of the allergen starting with tiny amounts
45
What are the mechanisms underlying desensitization?
Induction of regulatory T cells secreting IL-10 or TGF-B to skew the response away from IgE production Treat for allergic rhinitis Allergic asthma Venom allergy Drug Allergy

Immuno (7 decks)

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