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MMI 436 > Allergy and Asthma I > Flashcards

Allergy and Asthma I Flashcards

1
Q

What is a hypersensitivity?

A

over reaction of the immune response to certain foreign substances

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2
Q

What is allergy?

A

abnormal adaptive immune response directed against environmental substances (allergens)

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3
Q

What is atopy?

A

a genetic dispostiion to develop an allergic reaction (as allergic rhinitis, astham, or atopic deramatitis) and produce elevated levels of IgE upon exposure to an environmental Ag., especially when inhaled or ingested

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4
Q

What is anaphylaxis?

A

an allergic disorder; a serious life-threatening allergic rxn which usually occurs within minutes of exposure to allergens; systemic response –> high inflammation everywhere

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5
Q

Describe the pathologic immune mechanisms and mechanisms of tissue injury/disease for the following hypersensitivities:

  • immediate hypersensitivity: type 1
  • Ab mediated: type 2
  • immune complex mediated: type 3
  • T cell mediated: type 4
A
  • type 1: IgE –> mast cells and their mediators
  • type 2: IgM, IgG Abs against cell surface or ECM Ags –> opsonization and phagocytosis of cells; FcR and complement R-mediated recruitment and activation in leukocytes
  • type 3: immune complexes of circulating Ags + IgM or IgG Abs –> complement-and-FcR-mediated recruitment and activation of leukocytes
  • type 4: CD4 T cells (delayed-type hypersensitivity) –> MF activation, cytokine-mediated inflammation; CD8 T cells (T-cell mediated cytolysis) –> direct cell killing, cytokine-mediated inflammation
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6
Q

What type of macromolecules tend to be allergens?

A
  • mostly proteins (often proteases)
  • may also be lipids or carbs
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7
Q

What are the two main groups of allergens? Give examples

A
  1. IgG-dependent (e.g. grass or pollen)
  2. IgE-independednt –> directly activated the effector cells, usually causes dermatitis (e.g. poison ivy or nickel)
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8
Q

What is the exposome?

A

what you’ve been exposed to throughout your life

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9
Q

What are 5 commonalities that predispose a person to allergies?

A
  1. chronic inflammation
  2. environmental pathogens (e.g. chemicals, air pollution)
  3. altered microbiome
  4. food allergens in changed diet
  5. genetic predisposition
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10
Q

What causes allergies to develop?

A

associated with damage or dysregulation of the epithelial barrier (protects from the outside, so if damaged, can lead to allergy to what damaged it)

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11
Q

What is allergic sensitization/phase 1?

A
  • 1st exposure to an allergen that results in the devlopment of hypersensitivity
  • coating of mast cells with IgE
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12
Q

what happens when the early phase response is triggered?

A

rapily lead to release of pro-inflam mediators, e.g. histamine, tyrptase, prostaglandins, leukotrienes, and cytokines, which –> allergic symptoms (rhinorrhea, mucus secretion, bronchoconstriction, etc) and maybe even anaphalaxis

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13
Q

What is the last phase response?

A

characterized by the recruitment of further mast cells and eosinophils primary induced through IL-5, follows within several hours

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14
Q

Describe the steps of sensitization

A
  1. epithelial barrier disruption
  2. damages epithelial barrier releases alarmin and TSLP –> activated DCs and ILC2 cells
  3. activated DCs migrate to local LNs where they present allergen peptides to naive CD4 T cells on MHC-II
  4. recognition of these peptide/MHC complexes by the TCR induces differentiation of the Th2 subtype and production of Th2 cytokines (IL-4, 5, 13)
  5. IL-4/13 together with ligation of CD40/CD40L and CD80-86/CD28 induces Ig class switch in B cells and production of IgE
  6. IgE binds to the surface of cells that express high affinity FceRI (mast cells, basophils, eosiniophils)
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15
Q

Describe the steps of allergic inflammation

A
  1. when “sensitized” mast cells encounter the allergen, it crosslinks their FceRI and activates the release of many proinflammatory mediators (e.g. histamine)
  2. release of mast cell derived pro-inflam mediators CAN result in allergy symptoms
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16
Q

Describe the structure of high affinity FceRI

A
  • alpha chain: binds the C(H)3 domain of IgE with membrane proximal to alpha2 domain
  • beta chain: spans the membrane four times and has 1 ITAM in its cytoplasmic domain
  • two identical gamma chains: mostly intracellular, serving as the major transducing units, contains 2 ITAMs (one in each subunit)
17
Q

What is the role of ILC2s in asthma progression?

A
  1. pathogens damage epithelial damage –> alarmin relase (e.g. TSLP, IL-33)
  2. ILC2s are activated
  3. type 2 cytokine (IL-4, 5, 13) release –> eosinophil activation; repair epithelial tissue
18
Q

Where the Tregs at?

A
  • in some patients, subsets of Tregs aren’t functioning properly
  • tissue Tregs are functionally impaired in asthmatic children
19
Q

Describve IgE-independent allergy mechanism

A
  1. sensitization –> IgE on mast cells
  2. haptens bind to IgE –> cross links FceRI
  3. release of mast cell mediators
20
Q

What are mast cell and basophil origins? i.e. what gives rise to what

A

YSP –> mast cells
CMP –> basophils and mast cells

21
Q

Where are mast cells distributed?

A

under the mucosa layer, tissue residents - do not enter blood

22
Q

What is severe asthma?

A

continued asthma symptoms, frequently worsening of asthma symptoms and attacks among pateitns who take multiple astham meds with a high degree of compliance and good trigger management

23
Q

What are allergic diseases? examples and what is it associated with?

A

occur in the event of an exaggerated immune response to environmental allergens

mostly associated with the production of IgE

e.g. asthma, atopic dermatitis

24
Q

What is asthma?

A

chronic respiratory disease, which can be triggered by allergens, airway infections, pollutants

25
Q

What are the three major pathophysiologic components of asthma?

A
  1. bronchoconstriction
  2. airway inflammation
  3. bronchial hyperresponsiveness (twitchy airways)
26
Q

How is asthma diagnosed?

A
  • mediacal history
  • physical exam
  • spirometry - lung function tests
27
Q

What are the two key measurements of spirometery? Describe each, and what lower than normal readings indicate

A
  1. forced vital capacity (FVC): largest amount of air that you can forcefully exhale after breathing in as deeply as you can; lower reading –> restricted breathering
  2. forced expiratory volume (FEV): how much air you can force from your lungs in 1s; help assess severity; lower readings –> significant obstruction
28
Q

What are the different asthmatic phenotypes?

A
  1. non-atopic/instrinisc asthma
  2. atopic/extrinsic asthma
  3. disease severity: mild, moderate, and severe; corticosteroid-dependent and independent (depends how well they respond)
  4. other: triggers, age at onset, airflow obstruction
29
Q

What are the two endotypes of asthma?

A
  1. T2-high asthma: mostly driven by Th2 and ILC2 responses
  2. T2-low asthma: characterized by neutrophilic or paucigranulocytic (normal levles of eos and neutrophils) inflammation

MMI 436 (14 decks)

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