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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
what are some examples of primary mediators of IgE response?
histamines and proteases
26
what is meant by "secondary" mediators of IgE driven response?
synthesized in response to activation
27
what are 2 examples of secondary mediators of IgE response?
leukotrienes and prostaglandins
28
what is the function of leukotrienes?
increased vascular permeability, contraction of pulmonary smooth muscles
29
what are the functions of prostaglandins in allergy?
vasodilation, contraction of pulmonary smooth muscles, platelt aggregation
30
activated and degranulating mast cells have ___ and ___ impacts
delayed and immediate
31
the immediate responses of mast cells in allergy are inflammatory and act on what cell types?
second mediators (i.e. neutrophils, monocytes, platelets, T cells)
32
what are the acute changes caused by activated and degranulating mast cells?
increased vascular permeability, smooth muscle contraction and can lead to anaphylaxis
33
what is anaphylaxis?
a systemic life-threatening state including a drop in BP and contraction of muscles (including those in the lungs, which can impair breathing)
34
the chronic phase of activated and degranulating mast cells may involve ___ remodelling
tissue
35
what are the 3 phases of an allergic asthma response?
1. early response (immediate) 2. late-phase response (12hrs) 3. chronic response (3 dyas +)
36
what is the early response of an allergic asthma?
reflects a typical IgE response with vasodilation and bronchoconstriction and mucous production
37
what is the late-phase response in allergic asthma?
cytokines produced by activated mast cells recruit second mediators (i.e. eosinphils, neutrophils), which then recruit more leukocytes (more activation = more tissue damage)
38
what is the chronic response in allergic asthma?
basophils and fibroblasta promote chronic inflammation and tissue remodelling that impairs lung flexibility and function
39
what are some predisposing factors to allergy?
irritants, air pollution, cigarette smoke (including 2nd hand), low microbial diversity and low fibre diet
40
what are some protective factors against developing allergies?
exposure to microbes (ex: farm animals), probiotics, high microbial diversity & high fibre diet, and early exposure to these things
41
what is the hygeine hypothesis?
early exposure to pathogens and unsanitized environments calibrates the immune system to better know when something is a pathogen or not
42
what are 2 pieces of evidence for the hygiene hypothesis?
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
what are 4 pharm treatments for type 1 hypersensitivy?
1. antihistamines 2. leukotriene antagonists (ex; montelukast) 3. cortisone 4. epinephrin
44
what is the MOA of antihistamines in allergy?
block H1 and H2 receptors
45
what is the MOA of cortisone in allergy?
blocks degranulation through cAMP production, reduces histamine production
46
what is the MOA of epinephrine in allergy?
reverses effects of histamine on smooth muscle and vascular endothelial cells & stimulates cAMP levels in mast cells and basophils, blocking degranulation
47
what is hyposensitization therapy?
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
hyposensitization therapy may cause a shift to ___ response
Th1
49
what is the general process of type 2 hypersensitivity?
IgG or IgM mediated complement activation against inappropriate targets leading to ADCC and/ or phagocytosis
50
what is hemoyltic disease of the newborn?
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
what is given to prevent hemolytic dx of the newborn?
anti-Rh antibodies (RhoGAM)
52
does IgM have a role in hemolytic dx of the newborn?
it is too big to cross the placenta, so no
53
hemolytic dx of the newborn in a type __ hypersensitivity rxn
2
54
what is the MOA of type 3 hypersensitivity rxn?
Ag-Ab complexes deposited in various tissues induce complement activation and an inflammatory response mediated by neutrophils
55
what are the side effects/presentation of type 3 hypersensitivity rxn?
localized Arthus rxn and generalized rxns like serum sickness, necrotizing vasculitis, gelomerulonephritis, RA, SLE
56
what is the simplified MOA of type 3 hypersensitivity reaction?
antibody-antigen compexes (immune complexes) are not phagocytosed, but rather accumulate and may be deposited in blood/tissues
57
t/f type 3 hypersensitivity rxns can be systemic or localized
t
58
if the immune complexes of type 3 hypersensitivity accumulate, they can cause inflammation by binding to Fc receptors on what cell types?
mast cells, neutrophils, and macrophages
59
what are 4 outcomes of type 3 hypersensitivity reactions?
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
what are 4 propertoes of type 3 hypersensitivity antigens?
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
type 4 hypersensitivity is AKA ___
delayed type hypersensitivity (DTH)
62
how long is the "delay"in type 4 hypersensitivity?
1-2 days after exposure
63
what is the immune-cell MOA of type 4 hypersensitivity reactions?
sensitized T cells release cytokines that activate macrophages or Tc cells which mediate direct cellular damage
64
type 4 hypersensitivity is driven by activation of ___ and ___ immune responses
Th1 and Th17
65
what happens in chronic DTH?
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
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
tuberculosis
67
exposure to poison oak and the TB skin test are examples of ____ DTH reactions
short-term (cleared)
68
what are the 2 phases of type 4 sensitivity?
1. sensitization | 2. effector

Immunology PY2 (20 decks)

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