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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

what is the function of the immune system?

A

to provide a robust defence against a wide variety of aggressive external agents (mainly microorganisms)
and internal aggressive agents (e.g. cancer)

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2
Q

what is consequence of immune recongition?

A
  • intended destruction of antigen and collateral tissue damage
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3
Q

what is hypersensitivity definition?

A

immune response that results in bystander damage to self
- usually exaggeration of normal immune mechanisms
- pathophysiological basis for many chronic diseases including allergy & autoimmunity

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4
Q

what is Gel and Coombs classification?

A

-splitting of hypersensitivity into 4 types

Type I : Immediate hypersensitivity
Type II : Direct Cell effects
Type III : Immune Complex Mediated
Type IV : Delayed type hypersensitivity

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5
Q

what types of hypersensitivity are driven by antibodies?

A

Type I, II and III
(immediate hypersensitivity, direct cell effects, immune complex mediated)

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6
Q

what types of hypersensitivity are driven by T cells?

A

delayed type hypersensitivity (type $ only)

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7
Q

what are type 1 - immediate hypersensitivity reactions triggered by?

A

allergens e.g.
- House dust mite
- Pollen and animal dander
- Foods
- Drugs
- Latex
- Bee & wasp venom

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8
Q

what are allergens?

A

antigen that drives allergic reaction, many are soluble proteins that function as enzymes

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9
Q

what people are type 1 reactions prevalent in?

A

people who suffer from gentically predisposed so more likely to have lots of allergies

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10
Q

what type of antbiody is the only true allergic reaction response?

A

IgE mediated reaction

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11
Q

what does allergic IgE response cause?

A

atopic dermatitis, food allergy & allergic asthma

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12
Q

what are major players in type 1 hypersensitivity reaction?

A

IgE antibodies
mast cell degranulation in mast cells
effector T cells that are differentaited to CD4+
Eosinophil
B cell

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13
Q

what is the hygiene hypothesis?

A

in our modern westernised world, we’re too clean so develop allergies as from birth we’re not exposed to many allergies or parasites so never properly train our immune system

this means that in absence of parasitic infection, type 1 hypersensitivity reactions to innocuous (harmless) substances promote allergic reaction

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14
Q

what is Treg?

A

T regulatory cells -> t cells that regulate function of T & B cells in general

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15
Q

what are Th1 differentiation stimuli? what does that lead to? (from birth)

A

Th1 differentiation stimuli:
- older siblings (that are out in world)
-early daycare exposure
-rural environment
-childhood infections
-microbial pet exposure
- pets

= this means more balanced Treg activity and means Th2 is differentiated to Th1 (because of these stimuli) which means no allergies

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16
Q

what happens if lack of Th1 stimuli? what effect does this have? in what ways do babies/young children lack stimuli?

A
  • by being an only child
  • widespread use of ABX
    -urban environment with allergen sensitization -> dust mites & cockroaches

=this means lack of Th1 stimulim and redcued Treg activity so Th2 not differentiated to Th1 so has things like allergy & asthma

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17
Q

what drives sensitization phase?

A

Th2 effector cells

18
Q

what is the germinal centre?

A

a specialized microstructure that forms in secondary lymphoid tissues, producing long-lived antibody secreting plasma cells and memory B cells, which can provide protection against reinfection

19
Q

what is Tfh cells function?

A

they’re specialized providers of T cell help to B cells, and are essential for germinal center formation, affinity maturation, and the development of most high affinity antibodies and memory B cells.

20
Q

describe sensitisation stage of hypersensitivity type 1?

A

someone for example breathes in pollen and antigen presenting cell like macrophage or dendritic cell will present allergen derived peptide on MHC class II molecule and naive CD4+ T cell binds and

1.differentiates to Th2 cell which releases cytokines to switch B cell from producing IgM to IgE antibodies and will also release cytokines to stimulate eusinophils which release toxic granules
2. differentiates to Tfh cells which help B cells respond to allergen by releasing cytokines

then mast cells and basophils express receptors that bind to Fc region of IgE antibodies on their surface
- some residual IgE antibodies bind and this just means mast cells and basophils are geared up & ready

21
Q

what happens in pathological stage when re-encounter of the allergen?

A
  • Allergen binds to IgE-coated mast cells, &basophils→degranulation
  • Release of vasoactive mediators (histamine, tryptase)
  • Also increased expression of pro-inflammatory cytokines and leukotrienes
22
Q

what effects does histamine cause?

A

increased vascular permability (which affects blood pressure & breathing)
smooth muscle contraction

23
Q

what are generic features of symptoms of allergens?

A
  • occurs quickly after exposure to allergen (minutes to 1/2 hours)
  • responses are stereotyped
  • may be associated with more than 1 organ system
  • presentation is influenced by site of contact
  • threshold for reactions may be influenced by co-factors such as exercise, alcohol & infection
24
Q

what are specific symptoms from allergen?

A
  • asthma
  • Urticaria (hives - skin reaction)
  • Angioedema (tissue swelling)
  • Allergic rhinitis (hayfever)
  • Allergic conjunctivitis (sore eye)
  • Diarrhoea and vomiting
  • Anaphylaxis (severe type of allergic reaction)
25
Q

what is management of IgE mediated allergic disorders?

A
  • avoidance of allergen
  • block mast cell activation (prevents degranulation)
  • prevent effects of mast cell activation (anti-histamine & leukatrine receptor antagonists)
  • anti-inflammatory agents
  • adrenaline
  • immunotherapy
26
Q

what is immunotherapy?

A

trying to train immune system to tiny tiny doses and gradually over several years, immune system can be trained to go from Th2 to Th1 response → successful but dangerous & costly

27
Q

what is type 2 hypersensitivity mediated by?

A

IgM/IgG antibodies directed towards antigens present on cell surface or extracellular matrix

they either cause:
- destruction of antigen-positive cells
- stimulation of cell surface antigens

28
Q

what are the functions of antibodies?

A
  1. activate b lymphocytes
  2. acts as opsonin
  3. cause antigen clumping and inactivation of bacterial toxins
  4. activates antibody-dependant cellular activity
  5. triggers mast cell degranulation
  6. activates complement
29
Q

what is a type Ila reaction?

A

type 2 a of direct cell effects hypersensitivity reaction
= destruction of antigen positive cells

30
Q

what is type IIb reaction?

A

type 2 b of direct cell effect hypersensitivity reaction
= stimulation of cell surface antigen

31
Q

whats an example of type IIa reaction?

A
  1. opsonization & phagocytosis (cell)
  2. complement & Fc receptor-mediated endocytosis (it’s Fc receptor that binds at at least 2 heads on surface to activate complement system which leads to MAC destruction & inflammation)
32
Q

whats an example of type IIb reaction?

A

antibody mediated cellular dysfunction
- antibodies can bind to antigen and alter them
1. antibody can bind and stimulate receptor without hormone
2. antibody can inhibit binding of neurotransmitter to receptor

e.g. graves disease (hyperthyroidism), myasthenia gravis

33
Q

what is type 3 hypersensitivity?

A

immune complex mediated

-generate antibody against soluble antigen (not membrane bound-just floating around)

34
Q

what do antibodies do in type 3 hypersensitivity?

A

antibodies attach to soluble antigens and make large immune complex which means it’s easily phagocytosed

35
Q

what happens with small immune complexes in type 3 hypersensitivty?

A
  1. they’re less attractive to macrophages so stay in blood longer
  2. they move down and lodge in capillaries between the endothelial cells & basement membrane.
  3. where they activate complement proteins which through series of steps lead to vasodilation and cell death (via formation of the MAC
  4. complement proteins & antigen-antibody complexes attract neutrophils to the area
  5. the neutrophils discharge their killing agents & promote massive inflammation which leads to tissue death & hemorrhage
36
Q

what is difference in symptoms between type II and type III hypersensitivity?

A

type II depends on where the antigen-antibody is made
type III depends on where the immune complex is depositied

37
Q

where are immune complexes commonly deposited?

A

post-capillary venules or areas with small venules
in skin like kidneys

38
Q

what is clinical example of type III hypersensitivity?

A

acute hypersensitivity pneumonitis. immune complexes deposited in walls of alveoli & bronchioles

39
Q

what is type IV hypersensitivity mediated by?

A

T cell (CD4+)

type 4 = delayed type hypersensitivity

40
Q

what are the classical hallmarks of a type IV reaction?

A

-The large number of macrophages at the reaction site (accumulation of activated macrophage)

-That it takes an average of 24-48 hrs for symptoms to manifest after re-exposure to the initiating antigen (excluding sensitisation phase)

-Granulomas often form due to infectious pathogens/foreign bodies that cannot be cleared

41
Q

what are granulomas?

A

accumulation of macrophages

42
Q

what happens in type IV hypersensitivity reaction?

A

driven by CD4+ T cells
- activation of CD4+ T cells by an antigen which leads to proliferation & differentiation of effector Th1 cells leading to macrophage recruitment & activation
(CD8+ T cells & B cells may also be involved)

Immunology (6 decks)

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