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Microbiology & Immunity > 22 - Hypersensitive Reactions > Flashcards

22 - Hypersensitive Reactions Flashcards

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1
Q

what are the 4 types of hypersensitive reactions?

A

type 1 - immediate (IgE-mediated) hypersensitivity
type 2 - cytotoxic (IgG/IgM- mediated) hypersensitivity
type 3 - immune complex-mediated hypersensitivity
type 4 - delayed-type (cell-mediated) hypersensitivity

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2
Q

what is a hypersensitivity reaction?

A

an inappropriate or overreactive immune response to an antigen resulting in undesirable effects

symptoms typically appear in individuals who had at least one previous exposure to the antigen

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3
Q

examples of type 1 hypersensitivity

A

allergic rhinitis
asthma
anaphylaxis
skin prick test - testing for different allergens

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4
Q

examples of type 2 hypersensitivity

A

Graves’ disease
myasthesia gravis
autoimmune haemolytic anaemia

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5
Q

examples of type 3 hypersensitivity

A

systemic lupus erythematosus
serum sickness
Arthus reaction

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6
Q

examples of type 4 hypersensitivity

A

allergic contact dermatitis (e.g. to nickel, poison ivy)
tuberculin reaction
tuberculosis leprosy

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7
Q

what is type 1 hypersensitivity?

A

immediate reaction following exposure to an immune reactant like an environmental agent/ allergen - causes allergen-specific IgE responses

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8
Q

describe the mechanism behind type 1 hypersensitivity

A

exposure to an immune reactant/ allergen - presented by APCs as a soluble antigen in the context of MHC 2 to T-helper 2 cells

Th2 cells release IL-4 and 13 to activate B cells

activated B cells differentiate into plasma cells - secrete IgE specific to the allergen

IgE binds to mast cells and basophils via their Fc receptors - IgEs cross-link mast cells

results in mast cell activation and degranulation - release of leukotrienes, proteolytic enzymes and histamines

cause a localised inflammatory response such as allergic rhinitis, anaphylaxis, asthma

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9
Q

what is anaphylaxis? mechanism behind it associated with type 1?

A

anaphylaxis - severe, life-threatening facial swelling and oedema which leads to occlusion/ vasoconstriction of the resp tract, causes difficulty breathing

mechanism:
= with initial exposure/ sensitisation to an allergen - allergen-specific IgEs are produced
= following re-exposure - allergen binds to many IgEs on the surface of resident tissue mast cells and basophils - causes cross-linking of IgEs = mast cells activated
= mast cells degranulate - release leukotrienes, histamines, inflammatory mediators
= histamine, leukotrienes, and other mediators cause smooth muscle contraction, particularly in the bronchioles (bronchoconstriction) and swelling of the airways
= leads to respiratory distress, decreased perfusion

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10
Q

treatment for anaphylaxis and bronchoconstriction? mechanism?

A

treatment with immediate adrenaline via EpiPen

  • relaxes smooth muscles lining airways = bronchodilation
  • inhibits activation and degranulation of mast cells and basophils = reduces release of inflammatory mediates = dampens inflammatory response
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11
Q

what is type 2 hypersensitivity?

A

immune/ cytotoxic/ antibody-mediated hypersensitivity reaction

immune response characterized by the body’s own antibodies (IgG/IgM) mistakenly targeting its own cells or tissues, leading to cell destruction or dysfunction - interlinked with autoimmunity

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12
Q

describe the mechanism behind type 2 hypersensitivity

A

IgG and IgM antibodies produced against specific antigens on host cell surfaces - foreign or self antigens

binding of Ig-antigen leads to destruction of cell through various mechanisms:
1. activation of complement cascade via classical pathway = formation of MACs on target cell membrane leads to lysis
2. IgGs act as opsonins = opsonisation of host cells by antibodies, detected by macrophage Fc receptor binding to IgG Fc regions - facilitates phagocytosis
3. formation of immune complexes with antigen-antibody binding triggers inflammation and recruits immune cells like macrophages, neutrophils

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13
Q

describe how Graves’ disease is type 2

A

autoantibodies against TSH receptor on thyroid gland - bind and stimulate overproduction of thyroid hormone regardless of negative feedback of HPT axis

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14
Q

describe how myasthesia gravis is type 2

A

antibodies bind to Ach receptors - block Ach binding = block neuromuscular junction signalling between neurone and muscle for contraction

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15
Q

describe how (autoimmune) new-born haemolytic disease is type 2 - what is it? mechanism/ pathology? treatment?

A

haemolytic disease of new-born occurs when there’s a Rh blood group incompatibility between a RhD -ve mother and RhD +ve foetus

mechanism:
in pregnancy - RhD -ve mother is exposed to RhD +ve foetus = develops IgG antibody immune response against RhD +ve antigen of the foetus
= maternal IgG crosses placenta and enters foetal circulation
= binds to foetal RhD -ve antigens and leads to haemolysis of foetal RBCs by mother’s immune system

pathology:
- mild cases = anaemia, jaundice, mild hepatosplenomegaly
- severe cases = organ failure

treatment: if known beforehand, administer RhIg during pregnancy - binds and neutralises maternal RhD antigens, prevents immune response

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16
Q

what is type 3 hypersensitivity?

A

immune-complex mediated hypersensitivity – involves formation of immune complexes with IgGs and soluble antigens

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17
Q

describe the mechanism behind type 3 hypersensitivity

A

following initial exposure to an antigen - upon re-exposure, IgGs bind specifically to the soluble antigen and form immune complexes

immune complexes circulate and are deposited in various tissues - activate complement system and generate complement fragments like C3a and C5a

recruit immune cells - neutrophils and macrophages
= release inflammatory cytokines, contribute to inflammatory response
= macrophages recognise and engulf immune complexes - additional release of inflammatory cytokines

inflammation causes tissue damage - can manifest with localised inflammation, redness and swelling; manifestations depend on site of immune complex deposition

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18
Q

what is Arthus reaction?

A

localised immune complex mediated hypersensitivity reaction = causes local inflammation of small vessels/ vasculitis

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19
Q

mechanism behind Arthus reaction?

A

occur following high doses of (booster) vaccines - e.g. tetanus

-pre-existing IgG antibodies to vaccine bind to antigen of booster dose = form a large number of immune complexes due to high dose of vaccine
- immune complexes deposited in various tissues, activate complement system
- recruits inflammatory cells, releases inflammatory mediators = triggers inflammatory response that causes tissue damage
- results in local tissue destruction, vasculitis, localised swelling and redness

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20
Q

what is serum sickness?

A

caused by a large iv dose of soluble antigens - e.g. foreign proteins from meds/ drugs

IgG antibodies formed against specific antigen form many immune complexes due to antigen excess - deposited in tissues and triggers complement cascade via classical pathway = recruits inflammatory cells, release inflammatory cytokines, MAC formation induces cell lysis - tissue damage occurs

causes fever, rash, joint pain and sometimes organ dysfunction

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21
Q

what is farmer’s lung?

A

a type of hypersensitivity pneumonitis = leads to chronic inflammation, infiltration and damage to airways

occurs in people repeatedly exposed to organic dust from hay, straw = inhale airborne antigens like fungal spores, bacteria…

mechanism:
IgG binds to specific antigen - forms immune complexes which are deposited in walls of small airways/ bronchioles and alveoli - triggers an inflammatory response, recruits immune cells = leads to inflammation

effects:
with repeat exposure, leads to chronic inflammation, infiltration and damage to airways and lungs - lung fibrosis, bronchiolitis, flu-like symptoms, chronic progressive lung damage

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22
Q

where are the most common deposition sites for immune complexes following a large i.v. dose? what is the resulting disease?

A

blood vessel walls - vasculitis
renal glomeruli - nephritis
joint spaces - cause arthritis

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23
Q

where is the most common deposition site for immune complexes following a subcutaneous injection - e.g. booster dose? what is the resulting disease?

A

perivascular area

results in Arthus disease - localised inflammation

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24
Q

where is the most common deposition site for immune complexes following an inhaled antigen? what is the resulting disease? (type 3)

A

alveolar/ capillary interface, bronchioles/ small airways

farmer’s lung

25
Q

what are the two mechanisms for type 4 hypersensitivity?

A

Th1 mediated
Th2 mediated

26
Q

what is type 4 hypersensitivity?

A

delayed type - mediated by T cells, T helper cell activation and the release of pro-inflammatory cytokines & recruiting immune cells

27
Q

describe the Th1 mediated mechanism for type 4

A

following sensitisation - APCs present soluble antigen on MHC 2 to naïve CD4+ T helper cells

in response to specific cytokine environment (IL-2, IFN-gamma) = differentiates into Th1 cell

Th1 cell secretes pro-inflammatory cytokines like TNF-a, IFN-g, IL-2

recruits and activates other immune cells - macrophages and CD8+ T cells = release more inflammatory mediators, cause tissue inflammation - tissue damage and cell destruction

28
Q

example of type 4 Th1 mediated reaction?

A

tuberculin reaction

29
Q

describe the Th2 mediated mechanism for type 4

A

following sensitisation - APCs present soluble antigen on MHC 2 to naïve CD4+ T helper cells

in response to specific cytokine environment (IL4 & 5) - differentiates into Th2 cell

Th2 cells recognise APCs and become activated - secrete IL-4, 5, 13 = recruits and activates other immune cells - eosinophils, basophils and mast cells to site of antigen exposure

contribute to inflammation and immune responses characteristic of allergic reactions/ parasitic infections - eosinophil infiltration, mast cell degranulation, antibody-mediated responses

30
Q

example of type 4 Th2 mediated reaction?

A

allergic contact dermatitis

31
Q

why is type 4 delayed?

A

time course between 24-72 hours

32
Q

describe the type 1 Th1 mediated reaction for a Mantoux test - what is it?

A

Mantoux test = diagnostic test, determines if someone has been exposed to M. TB before

mechanism:
small amount of PPD with antigens from M.TB is injected intradermally into skin

from pre-exposure, memory T cells specific to M. TB recognise it, triggers an immune response, activates Th1 cells

Th1 cells release IFN gamma, TNF-alpha (pro-infl.), recruits other immune cells like macrophages to the site of injection

pro-inflammatory cytokines induce vasodilation, increase vascular permeability - increase blood flow, redness, swelling with fluid and proteins leaking out = localised inflammation with redness and swelling

size of swelling indicative of pre-exposure - larger swelling = higher chance of prior exposure to M. TB

33
Q

describe the type 4 response associated with tuberculoid leprosy/ Hansen’s disease - what is it? mechanism?

A

tuberculoid leprosy/ Hansen’s disease = infection with Mycobacterium leprae
- hypopigmented skin lesions, loss of sensation over skin lesions and affected nerves

mechanism:
strong Th1 response against M. leprae = activates and recruits macrophages, CD8+ & NK cells to site
- activated macrophages aggregate around antigens and form granulomas - organised collections of immune cells with isolate and contain the bacterial growth
- macrophages phagocytose and destroy bacteria

34
Q

what is an allergy?

A

disease following an immune response to an otherwise innocuous antigen – IgE mediated allergic reactions

35
Q

what is the response to systemic anaphylaxis?

A

oedema
increased vascular permeability
tracheal occlusion
circulatory collapse
potential death

36
Q

cause of acute urticaria?

A

animal hair
insect bites
allergy testing

37
Q

allergy response to acute urticaria?

A

local increase in blood flow and vascular permeability - redness and swelling

38
Q

what is IgE?

A

highly specific antibody; first line of defence against worms and parasites

39
Q

what receptors on mast cells do IgE bind to?

A

FcεR1 (Fc-epsilon-R1)

IgE pre-arms mast cells to react when in the presence of antigen

40
Q

function of IgE?

A

deals with multicellular parasites/ worms in a normal immune response

41
Q

mechanism against worms/ parasites - IgE mediated?

A

IgE binds to antigens on worm surfaces, activates mast cells & basophils

degranulation and release of inflammatory cytokines & toxic chemicals to kill parasites/ eliminate antigen

for parasites - chemicals also induce smooth muscle contractions - expels parasites from gut

42
Q

what are the two stages of allergic reactions?

A

initial exposure/ sensitisation
re-exposure

43
Q

describe the IgE-mediated response to initial allergen exposure

A

antigen is taken up be dendritic cells - processed and presented by MHC 2 to naïve CD4+ T cells

differentiation into Th2 cell is induced by specific cytokine environment (IL-4 & 5)

activated Th2 promotes B cell activation, differentiation into plasma cells and class-switching from IgM to IgE

IgE binds to FceR1 receptors on mast cells and basophils = high affinity binding - immune system is now sensitised with specific IgE for the specific allergen

following sensitisation - memory T cells and plasma cells maintain immunological memory of the allergen = allows for a quicker, exaggerated response next time

44
Q

describe the IgE-mediated response to allergen RE-EXPOSURE

A

allergen is detected and binds to specific IgEs already bound to mast cells - induces cross-linking of IgEs on mast cells

mast cells activated - degranulate and release:
- leukotrienes
- histamines
- proteolytic enzymes
- prostaglandins
- inflammatory mediators

induces various allergic symptoms:
- increased vasodilation & vascular permeability
- mucus secretion
- smooth muscle/ bronchoconstriction
- recruits inflammatory cells

contributes to - allergic rhinitis, asthma, anaphylaxis, urticaria

45
Q

what do degranulated mast cells release?

A

leukotrienes
prostaglandins
histamines
proteolytic enzymes
inflammatory mediators

46
Q

what somatic/ immune changes does mast cell degranulation induce?

A

increased vasodilation & vascular permeability
mucus secretion
smooth muscle/ bronchoconstriction
recruits inflammatory cells

47
Q

what influences degree of allergen sensitisation?

A

nature of allergen
- different allergens have different abilities to induce sensitization

dosage of allergen
- higher dosage = higher chances for sensitisation

location of priming
- site of initial allergen exposure & immune priming = e.g. initial exposure to allergen at mucosal surface instead of skin programs a different response

timing/ age
- early-life exposure has a greater impact on immune programming
- hygiene hypothesis

48
Q

what is the hygiene hypothesis?

A

reduced exposure to infectious agents during early childhood may lead to an increased risk of developing allergic and autoimmune diseases later in life

49
Q

list the genetic predispositions to allergy

A

environmental sensing - genetic factors influence how body detects environmental allergens, affects susceptibility

barrier function - genetic variants in genes encoding proteins as part of epithelial barriers

tissue response - variations in genes encoding cytokines, chemokines and receptors involved in inflammatory/ immune responses

atopic immune responses - dysregulated immune responses form overproduction of IgE, enhanced Th2 activity or aberrant cytokine production

50
Q

what is filaggrin? what’s its association to allergy responses?

A

filaggrin - filament-associated protein that binds to keratin fibres in epithelial cells; important in skin integrity

can become defective from genetic mutations in encoding gene - increases chances of atopic dermatitis

51
Q

list features of inhaled allergens that may promote Th2/ IgE responses

A

proteins - induce T cell responses

enzymatically active - often proteases

low dose - favours activation of Il-4 producing T cells

low molecular weight

highly soluble & stable

contains peptides that bind host MHC 2 - required for T cell priming

52
Q

what makes dendritic cells pro-allergenic?

A

thymic stromal lymphopoietin protein/ TSLP

53
Q

mechanism of TSLP influencing dendritic cells

A

TSLP is released by skin keratinocytes/ epithelial cells in response to injury, infection or allergen exposure

induces DCs towards a pro-allergenic phenotype by:

  • enhancing antigen presentation
  • increasing pro-inflammatory cytokine production
  • promote Th2 differentiation
  • promotes movement of DCs from tissues to lymph nodes

promotes allergic inflammation and sensitization

54
Q

two phases of allergic responses?

A

early and late phase

55
Q

what mediates the early phase of allergic interactions

A

mast cells

56
Q

what mediates the late phase of allergic interactions

A

T cells

57
Q

describe the early phase of allergic interactions

A

initiated immediately upon allergen exposure, mediated by mast cells with are sensitised by allergen-specific IgE

allergen cross-links IgE antibodies on mast cells = activation & degranulation

release of inflammatory mediators, leukotrienes, histamine - causes immediate allergic symptoms like itching, bronchoconstriction, hives, swelling…

58
Q

describe the late phase of allergic interactions

A

several hours after allergen exposure, can persist for days

prolonged sustained inflammatory reaction driven mainly by recruitment and activation of immune cells – esp. T cells

activated T cells into Th2 cells which produce IL-4, 5, 13 cytokines

cause chronic allergic reactions - e.g. allergic rhinitis, asthma, atopic dermatitis, eczema

Microbiology & Immunity (37 decks)

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