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Immunology PY2 > Lectures 27 & 28 > Flashcards

Lectures 27 & 28 Flashcards

1
Q

what is hypersensitivity?

A

an exaggerated and inappropriate immune response to an otherwise “harmless” antigen that leads to damaging pathology

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2
Q

hypersensitivity can results from ___ or ___ reactions

A

cellular or humoral

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3
Q

the type of hypersensitivity reaction is defined by what things?

A
  1. immunologic mediators

2. the characteristics of pathology, including the timing of reaction

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4
Q

what are the 4 types of hypersensitivity?

A
  1. Type 1 allergy & atopy
  2. Type 2 antibody mediated hypersensitivity
  3. Type 3 immune complex-mediated hypersensitivity
  4. Type 4 delayed-type hypersensitivity (DTH)
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5
Q

Type 1 (allergies) is mediated by what antibody type?

A

IgE

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6
Q

what is atopy?

A

a condition associated with increased propensity to produce IgE (typically genetic)

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7
Q

the gene loci for what features predispose a person to have atopy?

A
  1. MHC/HLA proteins
  2. innate immune receptors
  3. cytokines, chemokines, receptors
  4. FcREl alleles
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8
Q

allergic reactions occur in what 4 phases?

A
  1. priming
  2. sensitization
  3. activation
  4. effector
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9
Q

what happens in the priming stage of an allergic reaction?

A

allergen binds to BCR, B cells are co-stimulated by T cells and produce memory and plasma cells

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10
Q

what happens in the sensitization stage of an allergic response?

A

antibodies from the plasma cells bind to Fc IgE receptors on mast cells to sensitize them

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11
Q

what happens in the activation stage of an allergic reaction?

A

the sensitized mast cells sense the allergen when it is reintroduced and causes degranulation

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12
Q

what happens during the effector stage of an allergic response?

A

effects on smooth muscle, mucous glands, small BV, eosinophils etc.

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13
Q

during the priming stage of an allergic rxn, the damaged or inflammed epithelia enable initiation of _____ immune response

A

inflammatory

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14
Q

in the priming stage of an allergic rx, what cytokines promote a Th2 immune response that leads to IgE production?

A

IL-33, TSLP, and IL-25

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15
Q

in the priming stage of an allergic rxn, local ILC2s respond by making ___ and ___

A

IL5 and IL13

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16
Q

what is the function of IL5 and IL13 in the priming stage of the allergic rxn?

A

recruits eosinphils in the gut

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17
Q

during the priming stage of an allergic rxn, what is the role of IgE?

A

facilitates activation of mast cells and basophils

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18
Q

what are 5 common features of many allergens?

A
  1. highly soluble proteins/glycoproteins
  2. often more than one epitope
  3. may have enzymatic activities that allow access (i.e. disrupt epithelial barriers, stimulate protease-activated receptors
  4. contain pathogen-associated molecular patterns (PAMPs) which engage pattern recognition receptors
  5. enter mucosal surfaces at low concentrations, which favours Th2 immune responses
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19
Q

the high affinity ___ mediates allergy

A

FcERl

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20
Q

FcERI is expressed on what cell types? What do other immune cells express?

A

mainly mast cells, basophils, and eosinophils; other immune cells only express a and y chains and have lower affinity for IgE

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21
Q

FcERI regulates production of ___ by B cells

A

IgE

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22
Q

activation via the FcERI leads to what actions in the target cells?

A

target cell activation and degranulation

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23
Q

activation of target cells by the FcERI requires ____

A

cross-linking of at leat 2 RcERI receptors

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24
Q

what is meant by “primary” mediators of IgE driven respone?

A

pre-formed and released immediately on activation

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25
Q

what are some examples of primary mediators of IgE response?

A

histamines and proteases

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26
Q

what is meant by “secondary” mediators of IgE driven response?

A

synthesized in response to activation

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27
Q

what are 2 examples of secondary mediators of IgE response?

A

leukotrienes and prostaglandins

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28
Q

what is the function of leukotrienes?

A

increased vascular permeability, contraction of pulmonary smooth muscles

29
Q

what are the functions of prostaglandins in allergy?

A

vasodilation, contraction of pulmonary smooth muscles, platelt aggregation

30
Q

activated and degranulating mast cells have ___ and ___ impacts

A

delayed and immediate

31
Q

the immediate responses of mast cells in allergy are inflammatory and act on what cell types?

A

second mediators (i.e. neutrophils, monocytes, platelets, T cells)

32
Q

what are the acute changes caused by activated and degranulating mast cells?

A

increased vascular permeability, smooth muscle contraction and can lead to anaphylaxis

33
Q

what is anaphylaxis?

A

a systemic life-threatening state including a drop in BP and contraction of muscles (including those in the lungs, which can impair breathing)

34
Q

the chronic phase of activated and degranulating mast cells may involve ___ remodelling

A

tissue

35
Q

what are the 3 phases of an allergic asthma response?

A
  1. early response (immediate)
  2. late-phase response (12hrs)
  3. chronic response (3 dyas +)
36
Q

what is the early response of an allergic asthma?

A

reflects a typical IgE response with vasodilation and bronchoconstriction and mucous production

37
Q

what is the late-phase response in allergic asthma?

A

cytokines produced by activated mast cells recruit second mediators (i.e. eosinphils, neutrophils), which then recruit more leukocytes (more activation = more tissue damage)

38
Q

what is the chronic response in allergic asthma?

A

basophils and fibroblasta promote chronic inflammation and tissue remodelling that impairs lung flexibility and function

39
Q

what are some predisposing factors to allergy?

A

irritants, air pollution, cigarette smoke (including 2nd hand), low microbial diversity and low fibre diet

40
Q

what are some protective factors against developing allergies?

A

exposure to microbes (ex: farm animals), probiotics, high microbial diversity & high fibre diet, and early exposure to these things

41
Q

what is the hygeine hypothesis?

A

early exposure to pathogens and unsanitized environments calibrates the immune system to better know when something is a pathogen or not

42
Q

what are 2 pieces of evidence for the hygiene hypothesis?

A
  1. allergies are more common in western countries which are typically more sanitized
  2. newborns and children have immunity that is Th2 predominant and this is prolonged and stronger in children w/ allergies
43
Q

what are 4 pharm treatments for type 1 hypersensitivy?

A
  1. antihistamines
  2. leukotriene antagonists (ex; montelukast)
  3. cortisone
  4. epinephrin
44
Q

what is the MOA of antihistamines in allergy?

A

block H1 and H2 receptors

45
Q

what is the MOA of cortisone in allergy?

A

blocks degranulation through cAMP production, reduces histamine production

46
Q

what is the MOA of epinephrine in allergy?

A

reverses effects of histamine on smooth muscle and vascular endothelial cells & stimulates cAMP levels in mast cells and basophils, blocking degranulation

47
Q

what is hyposensitization therapy?

A

repeated SQ injections of the allergen to induce production of circulating allergen-specific IgG to remove allergen b4 it can trigger IgE sensitized mast cells and basophils

48
Q

hyposensitization therapy may cause a shift to ___ response

A

Th1

49
Q

what is the general process of type 2 hypersensitivity?

A

IgG or IgM mediated complement activation against inappropriate targets leading to ADCC and/ or phagocytosis

50
Q

what is hemoyltic disease of the newborn?

A

an Rh- mom can develop IgG antibodies against Rh+ child and those Ab can cross the placenta and cause the baby’s RBC to lyse, leading to jaundice as hemoglobin accumulates

51
Q

what is given to prevent hemolytic dx of the newborn?

A

anti-Rh antibodies (RhoGAM)

52
Q

does IgM have a role in hemolytic dx of the newborn?

A

it is too big to cross the placenta, so no

53
Q

hemolytic dx of the newborn in a type __ hypersensitivity rxn

A

2

54
Q

what is the MOA of type 3 hypersensitivity rxn?

A

Ag-Ab complexes deposited in various tissues induce complement activation and an inflammatory response mediated by neutrophils

55
Q

what are the side effects/presentation of type 3 hypersensitivity rxn?

A

localized Arthus rxn and generalized rxns like serum sickness, necrotizing vasculitis, gelomerulonephritis, RA, SLE

56
Q

what is the simplified MOA of type 3 hypersensitivity reaction?

A

antibody-antigen compexes (immune complexes) are not phagocytosed, but rather accumulate and may be deposited in blood/tissues

57
Q

t/f type 3 hypersensitivity rxns can be systemic or localized

A

t

58
Q

if the immune complexes of type 3 hypersensitivity accumulate, they can cause inflammation by binding to Fc receptors on what cell types?

A

mast cells, neutrophils, and macrophages

59
Q

what are 4 outcomes of type 3 hypersensitivity reactions?

A
  1. increased vascular permeability
  2. deposition of immune complexes in tissues
  3. complement activation (release of C3a and C5a)
  4. further recruitment, activation and tissue remodelling
60
Q

what are 4 propertoes of type 3 hypersensitivity antigens?

A
  1. multivalent & permit formation of 3D lattice structure
  2. high affinity for particular tissues
  3. highly charged (interfere with phagocytosis)
  4. defects in phagocytic system
61
Q

type 4 hypersensitivity is AKA ___

A

delayed type hypersensitivity (DTH)

62
Q

how long is the “delay”in type 4 hypersensitivity?

A

1-2 days after exposure

63
Q

what is the immune-cell MOA of type 4 hypersensitivity reactions?

A

sensitized T cells release cytokines that activate macrophages or Tc cells which mediate direct cellular damage

64
Q

type 4 hypersensitivity is driven by activation of ___ and ___ immune responses

A

Th1 and Th17

65
Q

what happens in chronic DTH?

A

there is a failure to clear the antigen/pathogen and can lead to a positive feedback loop of inflammation and may lead to tissue remodelling

66
Q

chronic DTH ay result in the formation of a granuloma, such as the one seen in _____ (dx) where the pathogen is walled off in a package surrounded by immune cells

A

tuberculosis

67
Q

exposure to poison oak and the TB skin test are examples of ____ DTH reactions

A

short-term (cleared)

68
Q

what are the 2 phases of type 4 sensitivity?

A
  1. sensitization

2. effector

Immunology PY2 (20 decks)

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