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MIIM30002 > Lecture 31: Immunopathology - Hypersensitivity and Allergy > Flashcards

Lecture 31: Immunopathology - Hypersensitivity and Allergy Flashcards

1
Q

What is type I hypersensitivity / what does this involve?

A

immediate hypersensitivity

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2
Q

What is type II hypersensitivity / what does this involve?

A

antibody mediated

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3
Q

What is type III hypersensitivity / what does this involve?

A

immune complex

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4
Q

What is type IV hypersensitivity / what does this involve?

A

delayed type hypersensitivity

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5
Q

What is allergy?

A

an immune-mediated inflammatory response to common environmental antigens that are otherwise harmless

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6
Q

What is atopy?

A

the enhanced tendency to produce IgE in response to environmental antigens

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7
Q

What are the tendencies of individuals with atopy?

A

have high levels of IgE (varies with condition)
large numbers of eosinophils
large numbers of IL-4 secreting Th2 cells

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8
Q

What are common features of allergens?

A

individuals are repeatedly exposed via a mucosal route
very stable
high solubility in bodily fluids
introduced in very low doses

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9
Q

What type of immune response do allergens induce?

A

a Th2 response

low dose, mucosal location

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10
Q

What are the different types of allergic reactions (type I hypersensitivity)?

A

systemic anaphylaxis, allergy rhinitis (hay fever), asthma (acute, chronic) and food allergies

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11
Q

What can type I hypersensitivity be separated into?

A

two phases which are sensitisation and response

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12
Q

What are examples of local and systemic responses?

A

local: rhinitis, bronchoconstriction and conjunctivitis
systemic: anaphylaxis

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13
Q

How does sensitisation occur?

A

the allergen leaves occludin in tight junctions and enters mucosa -> DC primes T cell in lymph node -> plasma cell travels back to mucosa and produces allergen-specific IgE antibodies

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14
Q

How does an allergic response occur?

A

allergen-specific IgE binds to mast cell; triggers mast cell degranulation

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15
Q

What causes degranulation?

A

multivalent antigen cross-links bind IgE antibodies

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16
Q

What does activation of mast cells result in?

A

secretion of preformed mediators (histamine)
synthesis and secretion of lipid mediators (prostaglandins and leukotrienes)
synthesis and secretion of cytokines (IL-3, IL-4, IL-13, IL-5)

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17
Q

What are the physiological effects of mast cell degranulation in the GI tract?

A

increased fluid secretion and peristalsis

diarrhea, vomiting

18
Q

What are the physiological effects of mast cell degranulation in the airways?

A

decreased diameter and increased mucus secretion

wheezing, coughing, phlegm

19
Q

What are the physiological effects of mast cell degranulation in the blood vessels?

A

increased blood flow and permeability

increased cell and protein, fluid in tissue, lymph flow and effector response

20
Q

What occurs during the immediate allergic response?

A

redness, vasodilation
soft swelling, leakage of plasma from venules
dependent upon IgE

21
Q

What causes the symptoms of the immediate response?

A

preformed mediators (histamines, etc) which are rapidly metabolised

22
Q

What occurs during the late allergic response?

A

hard swelling, accumulation of leukocytes
neutrophils, Th2 cells, eosinophils
occurs after 8-12 hours

23
Q

What causes the symptoms of the late response?

A

induced mediators (chemokines, cytokines, leukotrienes)

24
Q

What are the two outcomes of type II hypersensitivity?

A

injury due to activation of effector mechanisms or abnormal physiological response

25
Q

Activation of which effector mechanisms causes injury?

A

the complement cascade
recruitment of inflammatory cells
activation via Fc receptor

26
Q

What causes an abnormal physiological response?

A

binding to receptors or proteins interfering with function

activation or inhibition

27
Q

What is haemolytic disease of the newborn caused by?

A

preformed maternal IgG antibodies which react against the child’s Rh antigens on their RBC’s in utero -> removal of RBC via complement activation

28
Q

How is haemolytic disease of the newborn treated?

A

providing anti-Rh antibodies to the mother within 24 hrs of delivery to remove fetal RBC’s in maternal circulation

29
Q

When does type III hypersensitivity occur?

A

if complexes composed of self or foreign antigen are excessively produced, and inefficiently cleared

30
Q

What does the severity of type III hypersensitivity depend on?

A

depend on size and amount

depend on affinity and isotype of antibody

31
Q

What does the pathology of type III hypersensitivity depend upon?

A

where complexes are deposited e.g. cationic antigen complexes bind to blood vessels and kidney glomeruli (SLE)

32
Q

How are immune complexes removed?

A

small Ag:Ab complexes form in the circulation and activate complement -> many molecules of C3b are bound covalently to the complex -> bound C3b binds to CR1 on erythrocyte surfaces -> in the spleen and liver, phagocytic cells remove the immune complexes

33
Q

What happens when immune complexes are not cleared?

A

neutrophil activation / complement activation / mast cell degranulation
increased blood vessel permeability / blood flow
activation of platelets results in occlusion of vessels

34
Q

What is vasculitis caused by?

A

immune complex deposition in blood vessel walls

35
Q

What is glomerulonephritis caused by?

A

immune complex deposition in kidney basement membranes

36
Q

What is arthritis caused by?

A

immune complex deposition in joint synovium and vessels

37
Q

What are the mediators of type IV hypersensitivity?

A

heavy involvement of T cells (and macrophages)

classically CD4+ Th1 but sometimes CD8+ CTL

38
Q

What is type IV hypersensitivity elicited by?

A

microbial infection, intradermal injection of protein antigens or contact with chemicals (absorbed through skin)

39
Q

What occurs during type IV hypersensitivity sensitisation?

A

antigen penetrates the skin and is taken up by local antigen presenting cells -> dendritic cell primes T cell in lymph node

40
Q

What occurs during type IV hypersensitivity response?

A

re-exposure to antigen: Th1 recognises antigen and releases cytokines -> recruitment and activation of phagocytes and plasma to site of antigen exposure causes a visible lesion

41
Q

What is the purpose of a tuberculin skin test (Mantoux test)?

A

detects the presence of Mtb-specific CD4 T cells (an example of type IV hypersensitivity)

MIIM30002 (25 decks)

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