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Immunology > Allergy and the Immune Response to Parasites > Flashcards

Allergy and the Immune Response to Parasites Flashcards

1
Q

Why are multicellular parasites difficult to eradicate? (3)

A
  1. They are less antigenic
  2. Cannot be engulfed
  3. Have a long life-span
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2
Q

What are the functions of IL-4? (2)

A
  1. Induce differentiation of TH2 cells
  2. Induce claSs-switching to IgE
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3
Q

IgE binds to what receptor on mast cells, basophils, or activated eosinophils?

A
  • FcεRI (R1) - high affinity
  • FcεRII (R2) - low affinity
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4
Q

How long can IgE remain in serum after binding to R1 or R2?

A
  • Months to years
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5
Q

The R1 receptor is a tetramer where the α-chain is responsible for _____, and the β, γ, and γ chins are responsible for _____

A
  • Binding IgE
  • Signaling
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6
Q

B-cells have 50,000 to 100,000 receptors that are ______, whereas mast cells with bound IgE can have >500,000 R1 receptors that are _______

A
  • Monospecific
  • Polyspecific
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7
Q

Mast cells secrete the remodeling enzyme ______ in mucosal tissue and ______ in connective tissue.

A
  • Tryptase
  • Chymotryptase
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8
Q

When a pathogen binds TLR, it secretes IL-4 and IL-13 to amplify _____ and IL-5 for _____.

A
  • TH2 response
  • Eosinophil production/activation
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9
Q

What are the preformed mediators contained in the granules of mast cells?

A
  1. Tryptase (or chymotryptase)
  2. Histamine and/or heparin
  3. TNF-α
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10
Q

What are the biological effects of histamine and heparin?

A
  1. Poison parasites
  2. Increase vascular permeability
  3. Cause smooth muscle contraction

Overall triggers inflammation

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11
Q

What are the biological effects of TNF-α stored in granules of mast cells?

A
  1. Promote inflammation
  2. Stimulate cytokine production by many cell types
  3. Activates endothelium (induces expression of adhesion molecules)
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12
Q

What are mast cell mediators are synthesized after degranulation?

A
  1. IL-4 and IL-13
  2. IL-3, IL-5, GM-CSF
  3. CCL13
  4. Leukotrienes and prostaglandins
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13
Q

Where are the following histamine receptors located? H1, H2, H3, and H4

A
  • H1 - vascular endothelial cells, smooth muscle cells, heart, and brain
  • H2 - vascular endothelium and GI
  • H3 - CNS
  • H4 - Bone marrow
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14
Q

Prostaglandins and leukotrienes are formed from what common precursor present in cell membranes?

A

Arachidonic acid

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15
Q

What are the functions of prostaglandins in smooth muscle, endothelial cells in blood vessels, and neutrophils?

A
  • Smooth muscle - constriction
  • Endothelial cells - vasodilation
  • Neutrophils -chemotaxis
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16
Q

True or false. Aspirin blocks prostaglandin and leukotriene synthesis to help reduce inflammation.

A

False. It only blocks prostaglandins, not leukotrienes

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17
Q

What is the biological effect of CCL13 expressed by mast cells after degranulation?

A

Attraction of monocytes, macrophages, and neutrophils

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18
Q

In the context of IgE, why are mast cells more variable than B cells in terms of their response to antigen

A

Because mast cells bind to different IgE molecules of various specificities for antigen that can be diverse in their structure and biological origin

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19
Q

Which of the following have biological activities in common with histamine but are more potent?

  1. Prostaglandins
  2. Arachidonic acid
  3. Carboxylpeptidases
  4. Heparin
  5. Leukotrienes
A

Leukotrienes - about 100x more potent

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20
Q

Which forms of hypersensitivity reactions are antibody-mediated and which are T-cell mediated

A
  1. Type I: immediate - antibody
  2. Type II: cytotoxic - antibody
  3. Type III: immune complex - antibody
  4. Type IV: Delayed - T-cell mediated
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21
Q

Hypersensitivity reactions occur when an already immune or ______ individual is re-exposed to the initiating substance (allergen).

A

Sensitized

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22
Q

Explain the tenents of the hygiene hypothesis

A
  • Excessive hygiene reduces childhood exposure to pathogens
  • Vaccination reduces developing immune system’s experience in facing natural infections
  • Overreliance on antibiotics to terminate infections
23
Q

Type I hypersensitivities are mediated by ____ in response to allergens and usually occur within minutes

A

IgE

24
Q

What features of inhaled allergens promote priming of TH2 cells that drive IgE response.

A
  • Many allergens are proteases
  • Low molecular weight
  • High solubility
  • High stability
  • Contains peptides that bind to MHC-II
25
Q

What genetic and environmental factors can predispose an individual to type I hypersensitivity? (3)

A
  1. Structural variations in MHC-II enhances presentation of allergen-derived peptides
  2. TCR α-locus noncoding variant can enhance T-cell recognition of certain allergen-derived peptides
  3. Variations in expression of IL-4
26
Q

Describe the 3 stages of type I hypersensitivity reactions

  1. Sensitization
  2. Immediate rxn
  3. Late-phase rxn
A
  1. Sensitization - first exposure to allergen; IgE binds to mast cells and basophils
  2. Immediate rxn - second exposure; allergen triggers cross-linking of IgE and degranulation (~10 minutes)
  3. Late-phase - synthesis of prostaglandins and leukotrienes (~8 hours)
27
Q

What are the functions of eosinophils in the late-phase reaction of a type I hypersensitivity reaction?

A
  1. Release toxic granular proteins (tissue injury)
  2. Amplify inflammatory response with chemokines, prostaglandins, or leukotrienes
28
Q

When allergens enter the blood, it triggers ______

A

Systemic anaphylaxis

29
Q

What are the symptoms of anaphylatic shock?

A
  1. Urticaria
  2. Nausea/vomitting
  3. Rapid drop in bp due to vasodilation
  4. Difficulty breathing
  5. Organ damage
30
Q

What are haptens?

A

Molecules too small to invoke an immune response

Ex: penicillin

31
Q

What is meant by “wheal & flare”?

A

Urticaria and angioedema

32
Q

Inhalled allergens of the UPPER airway leads to ______

A

allergic rhinitis of the nasal passages and conjunctiva

33
Q

Inhalled allergens of the LOWER airways leads to _____

A

asthma

34
Q

Desensitization to an allergen involves giving a series of small injections of allergen to mount an immune response. Why does this work?

A

When allergen enters the blood stream, it then binds to IgG before it can bind to IgE and trigger systemic anaphylaxis.

35
Q

What is the function of Omalizumab (Zolair)?

A

Anti-IgE monoclonal antibodies used to treat type I hypersensitivity

36
Q

What is the function of Mepolizumab?

A
  • Monoclonal antibody against IL-5
  • Inhibits eosinophils
37
Q

_____ hypersensitivity reactions involve IgG or IgM against cell structures, resulting in destruction of the cell via complementation, opsonization, or antibody-dependent cellular toxicity (ADCC).

A

Type II

38
Q

Improper transfusion of blood types (ABO and Rh antigens) results in a ______ hypersensitivity reaction.

A

Type II

39
Q

What are isohemagglutinins?

A

IgM antibodies directed against blood group antigens

40
Q

First and subsequent pregnancies of Rh- mothers carrying Rh+ fetus are infused with _____, an anti-Rh IgG.

A

RhoGam

41
Q

Type III hypersensitivity is caused by _____

A

deposition of immune complexes

42
Q

Where are immune complexes most likely to deposit in type III hypersensitivity? (3)

A
  1. Blood capillaries
  2. Lung alveoli
  3. Kidney Glomeruli
43
Q

The adverse effects of immune-complex deposition are a direct result of _______ and subsequent accumulation of _______

A
  • Complement activation (C3a and C5a)
  • Neutrophil and platelet infiltration
44
Q

A penicillin allergy would be considered a type ____ hypersensitivity?

A

Type III

45
Q

What are the consequences to immune complex deposition in the following locations:

  1. Blood vessels
  2. Basement membranes of kidneys
  3. Basement membranes of joints
  4. Skin
A
  1. Blood vessels → vasculitis
  2. Basement membranes of kidneys → glomerulonephritis
  3. Basement membranes of joints → arthritis
  4. Skin → urticaria
46
Q

Type IV hypersensitivity reactions are mediated by _____

A

Antigen-specific TH1 cells

47
Q

Type IV hypersensitivity reactions typically occur ____ after exposure to antigen

A

1-3 days

48
Q

TH1 cells cause damage in type IV hypersensitivity reactions by secreting IFN-γ and TNF-β. What are the consequences of this?

A
  • IFN-γ - activation of macrophages
  • TNF-β - tissue destruction, macrophage activation, macrophage chemotactic factor
49
Q

A nickel allergy is an example of a type ___ hypersensitivity

A

Type IV

50
Q

How would a type IV hypersensitivity reaction present histologically?

A
  • Macrophage and T-cell infiltrates
  • Granuloma formation
  • “erythema and induration”
51
Q

Contact dermatitis is an example of a type ____ hypersensitivity

A

Type IV

52
Q

In order for a hapten to trigger contact dermatitis, it must be able to _____ (2)

A
  1. Penetrate the skin
  2. Covalently couple with host proteins
53
Q

What are the most common causes of contact dermatitis? (6)

A
  1. Organic chemicals
  2. Metals
  3. Topical drugs
  4. Cosmetics
  5. Plant material

Immunology (13 decks)

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