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Foundations Exam 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What mediates the four types of hypersensitivity reactions?

A

Type I: IgE (Th2)
Type II: Ab- mediated cytotoxicity (Th2)
Type III: immune complex (Th2)

Type IV: delayed (Th1)

*remember your ABCD:
I = Allergic Anaphylaxis
II = antiBody
III = immune Complex
IV = Delayed

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2
Q

Type I hypersensitivity

A

allergic reaction - exaggerated response to an antigen

immediate reaction

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3
Q

Type I hypersensitivity mechanism

A
  1. DC activates naive T cells —> Th2
  2. Th2 secretes IL-4 —> IgE class switching in B cells
  3. IgE binds Fc on mast cells and basophils
  4. upon secondary exposure - mast cells cross link surface IgEs, release inflammatory mediators: vasoactive (immediate) and cytokines (late phase)
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4
Q

these cells provide defense against parasitic worms and protozoa, and their products attract eosinophils. What are?

A

mast cells

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5
Q

what are primary (immediate) allergy mediators?

A

(pre-made/ stored):
- histamine and serotonin - vascular permeability, smooth muscle contraction
- neutrophil and eosinophil chemotaxis mediators

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6
Q

what are secondary allergy mediators?

A

secondary (synthesized in minutes):
- leukotrienes - vascular permeability, smooth muscle contraction
- prostaglandins - vasodilation, smooth muscle contraction, platelets activation
- bradykinin - vascular permeability, smooth muscle contraction, pain
- cytokines - recruit WBC, inflammation (causing late phase reaction)

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7
Q

what are the allergy mediators of late phase allergic reaction?

A

late phase (recruitment, up to 24hs):
- neutrophil and eosinophil inflammation
- protease damage

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8
Q

what are the allergy mediators of primary, secondary, and late phase reaction?

A

primary:
- histamine and serotonin
- neutrophil and eosinophil chemotaxis mediators

secondary:
- leukotrienes
- prostaglandins
- bradykinin
- cytokines

late phase:
- neutrophils and eosinophils
- protease damage

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9
Q

local vs systemic anaphylaxis manifestations

A

local: allergic rhinitis, asthma, urticaria (hives), eczema (atopic dermatitis), angioedema (swelling of soft tissue like lips)

systemic: disseminated mast cell activation results in increased vascular permeability, constriction of smooth muscle (—> extravasation of fluid, leading to hypotension), airway constriction, epiglottis swelling

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10
Q

when skin testing for an allergy, what will happen if a small amount of allergen is introduced (via intradermal injection or superficial scratching) to a patient with an allergy?

A

local mast cells will degranulate and cause increased permeability and fluid loss —> resulting in swelling (wheal)
and localized increased blood flow —> causing redness (flare)

so wheal (edema) + flare (red) = allergic

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11
Q

RAST allergy test

A

radioallergosorbent test (RAST): detects levels of IgE

  1. allergens coupled to beads
  2. serum is added, IgE binds beads
  3. labeled anti-IgE measures IgE levels
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12
Q

what happens on a molecular level as desensitization to an allergy occurs?

A
  • decreases Th2
  • induces Tregs
    —> IL-10 and TGF-b
    —> decreased IgE, suppressed mast cells, class switching to IgG and IgA
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13
Q

hygiene hypothesis (allergy)

A

developing immune system does not have enough contact with the right viruses and bacteria, so Th1 reactions are not sufficiently stimulated

immune system becomes unbalanced, with overactive Th2 response

solution: exposure to diverse environmental antigens may prevent sensitization to antigens

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14
Q

Type II hypersensitivity mechanism

A

antibody-dependent cell toxicity (ADCC) - IgM or IgG dependent
1. classical complement pathway activated
2. opsonization (IgM > IgG)
3. phagocytosis (macrophage, neutrophils)

takes a few hours (not immediate)

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15
Q

ADCC

A

antibody-dependent cell-mediated cytotoxicity: target cell opsonized, then lysed by cytolytic effector cells (NK primarily, some macrophage/neutrophils, eosinophils if parasitic/worm)

does not involve complement

dependent on prior antibody response

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16
Q

transfusion reactions, hemolytic disease of the newborn, autoimmunity, and drug-induced hemolytic anemia are type ____ hypersensitivity reactions

A

Type II: antibody-mediated cytotoxicity (via ADCC)

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17
Q

why does it make sense than IgM is better at opsonization than IgG?

A

IgM is a pentamer (more places to bind)

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18
Q

Graves’ disease (hyperthyroidism) is a Type ___ hypersensitivity

A

Type II (ADCC) hypersensitivity - leads to antibody-mediated activation of TSH (thyroid-stimulating hormone) receptors

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19
Q

myasthenia gravis is a Type ___ hypersensitivity

A

Type II (ADCC) hypersensitivity - antibodies inhibit Ach binding to receptors, leading to down-regulation of Ach receptor —> muscle weakness and paralysis

20
Q

Rheumatic fever is a Type ___ hypersensitivity

A

Type II (ADCC) hypersensitivity - causes inflammation and macrophage activation

antibody for streptococcal cell wall antigen cross-reacts with myocardial antigen —> myocarditis, arthritis

21
Q

Type III hypersensitivity

A

mediated by immune complex - caused by circulating antigen-antibody complexes —> lodge in small vessels and filtering organs

large complexes can be phagocytosed via complement, but small complexes get into tissues

takes 4-12 hours

22
Q

Type III hypersensitivity mechanism

A

mediated by antigen-antibody complex (usually IgG):
- large complex—> complement activation, phagocytosis
- small complex—> accumulate in blood, get into tissues

C3a and C5a (anaphylatoxins) induce inflammatory response —> neutrophils recruitment (phagocytosis), lytic enzyme (tissue injury), platelet activation (thrombosis)

23
Q

Arthus reaction

A

acute reaction initiated by local deposition of immune (Ab/Ag) complexes (as in Type III hypersensitivity)

takes 4-12 hours to develop - immune complexes must form and activate mast cells/ neutrophils/ complement

[faster than Type IV, but slower than Type I]

24
Q

what is an example of localized and systemic Type III hypersensitivity reactions?

A

Type III - mediated by Ab/Ag complex

localized:
- local deposition of complex in blood vessels
- insect bites
- drugs/vaccines (—> Arthus rxn)
- inhaled bacterial spores/ fungi (Farmer’s lung)

systemic:
- serum sickness (circulating immune complexes)
- autoimmunity (autoantigens) - SLE (systemic Lupus erythematosus), rheumatoid arthritis

25
Q

Farmer’s lung is a type ___ hypersensitivity

A

Type III (Ab/Ag) mediated

intrapulmonary reaction due to inhaled bacterial spores or fungi

26
Q

serum sickness is a type ___ hypersensitivity

A

Type III (Ab/Ag) - circulating immune complexes

27
Q

SLE and rheumatoid arthritis are both a type ____ hypersensitivity

A

Type III (Ab/Ag mediated)

SLE (systemic lupus erythematosus) and rheumatoid arthritis are both autoimmune diseases

28
Q

Type IV hypersensitivity

A

delayed - symptoms begin 24h after exposure, peaks between 48 and 72 hours

mediated by antigen-specific Th1 cells, antibody independent

major injury due to inflammation - CD4 Th, cytokines, T cell cytotoxicity

29
Q

how do Th1 cells induce Type IV hypersensitivity?

A

Type IV - delayed, antibody independent

Th1 secrete inflammatory cytokines, activate neutrophils and macrophages, recruit monocytes/macrophages/granuloma formation

Th1 can activate CTL (CD8+) killing

30
Q

Type IV hypersensitivity mechanism

A
  1. Th1 activation via MHC II APC and IL-12
  2. Th1 secrete INF-y —> activates macrophages
  3. macrophages produces IL-1, IL-6, IL-23
  4. activated Th17 recruit neutrophils via IL-17
31
Q

what happens upon secondary exposure in Type IV hypersensitivity (Th1 mediated)

A

memory T recognize antigen, secrete inflammatory cytokines, recruit macrophages (—> tissue damage) and neutrophils

macrophages —> granulomatous inflammation

CD8+ —> cytotoxicity

symptoms begin 24h after secondary exposure and peak between 48 and 72 hours

32
Q

what occurs following skin test for type IV hypersensitivity?

A

Type IV is delayed, so reactivity is evident between 48 and 72 hours

skin lesions form as a result of infiltration of inflammatory cells to site

[remember in skin test, antigen is introduced via intradermal injection or scratching]

33
Q

what kind of hypersensitivity reaction is utilized in diagnosis of tuberculosis?

A

Type IV (delayed - remember that you return for reading 48-72 hours later!)

positive Type IV reaction in dermis indicates prior exposure

34
Q

allergy to metal salts or other haptens causing contact dermitis to coins, jewelry, or nickel is an example of type ___ hypersensitivity

A

Type IV (delayed, Th1 mediated)

35
Q

urushiol, or poison ivy, is an example of Type ___ hypersensitivity

A

Type IV (delayed, Th1 mediated)

36
Q

which type of hypersensitivity is anaphylactic?

A

Type I (IgE mediated) - immediate reaction

37
Q

which of these is a type of Type I hypersensitivity?
a. Arthus reaction
b. Hay fever
c. ABO mistmatch
d. contact dermititis

A

b. Hay fever: type I (IgE, anaphylactic) hypersensitivity

Arthus rxn: Type III
ABO: Type II
contact dermititis: Type IV

38
Q

which of these is a type II hypersensitivity?
a. Arthus reaction
b. Hay fever
c. contact dermititis
d. Rh hemolytic disease of newborn

A

d. Rh hemolytic disease: Type II hypersensitivity (as is ABO mismatch) - ADCC mediated

Arthus rxn: Type III
Hay fever: Type I
contact dermititis: Type IV

39
Q

from this list, pick out the Type II hypersensitivities:
a. chronic transplant rejection
b. ABO mistmatch/ Rh (newborn)
c. contact dermititis
d. Graves’
e. hyperacute transplant rejection
f. allergy
g. myasthenia gravis
h. rheumatic fever
i. tubercular lesions
j. hemolytic anemia

A

Type II (ADCC) hypersensitivity:
b. ABO/Rh
d. Graves’
e. hyperacute transplant rejection
g. myasthenia gravis
h. rheumatic fever
j. hemolytic anemia

40
Q

a farmer’s respiratory problems related to an allergy to moldy hay is indicate of type ____ hypersensitivity

A

type I (anaphylactic/allergy)

41
Q

a chest x-ray showing nodular opacities in both lung apices is indicative of type ____ hypersensitivity

A

type IV (cell mediated) - granulomas form in tissues

42
Q

hay fever is a type ____ hypersensitivity

A

type I (anaphylactic)

43
Q

A patient comes into the emergency room with severe bleeding due to a car accident. They need a transfusion right away, but their blood type on file is wrong and they begin to experience a type ___ hypersensitivity

A

type II (cytotoxic/ADCC) hypersensitivity

44
Q

A patient complains of allergy symptoms that begin to occur a few hours after they arrive to work, at a factor that processes natural fibers. Their symptoms improve on the weekends. This is indicative of a type ___ hypersensitivity

A

Type III (immune complex) hypersensitivity

this is describing Farmers lung - reaction to spores in fibers

45
Q

Which products of activated complement bind to receptors on mast cells and stimulate release of inflammatory mediators?

A

C3a and C5a

46
Q

A boyscout allergic to poison ivy develops an itchy rash 2 days after a camping trip. What process below plays the largest role in this type of reaction?
a. CD8+ CTL killing
b. CD4+ Th cytokine secretion
c. proliferation of NK cells
d. activation of neutrophils

A

b. CD4+ Th cytokine secretion

remember that Type IV hypersensitivity is mediated by Th1

47
Q

Six months after transplantation, a transplanted kidney shows signs of acute rejection. What immune mechanism is responsible?
a. deposition of immune complexes
b. IgG production
c. anti-ABO antibodies
d. mast cell degranulation
e. cell-mediated immune response

A

e. cell-mediated immune response (T cell mediated) to donor MHC antigens not present in the recipient

Foundations Exam 2 (42 decks)

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