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lolmyi > L24: Hypersensitivity > Flashcards

L24: Hypersensitivity Flashcards

1
Q

What are the 4 types of hypersensitive reactions?

A

→Type 1: immediate hypersensitivity

→Type 2: cytotoxic hypersensitivity

→Type 3: serum sickness and Arthus reaction

→Type 4: delayed-type hypersensitivity, contact dermatitis

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2
Q

Describe Type I allergy reaction

A

→Initial exposure to the antigen causes the priming of Th2 cells, and their release of IL-4 causes the B cells to switch their production of IgM to IgE antibodies which are antigen-specific

→IgE antibodies bind tomast cellsand basophils, sensitising them to the antigen

→When the antigen enters the body again, it cross links theIgEbound to the sensitised cells, causing the release of preformed mediators

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3
Q

What should be included in a skin prick test?

A

→positive control

→negative control

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4
Q

What does Type 2 hypersensitivity reactions respond to?

A

→altered components of human cells

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5
Q

Give 4 example of a type 2 hypersensitivity

A

→penicillin modifies proteins on human erythrocytes to create foreign epitopes

→Grave’s disease

→myasthenia gravis-Antibodies block or destroynicotinic acetylcholine receptorsat thejunction between the nerve and muscle

→– Hemolytic disease of the newborn

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6
Q

Describe type 2 cytotoxic hypersensitivity

A

→Antibodies binding to cells can activate the complement system, leading to degranulation ofneutrophils

→Antibody-bound cells are cleared by:
FcgR+ cells such as macrophages

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7
Q

What is a special case of Type 2 response?

A

→involves IgG antibodies directed at cell-surface receptors

→ these antibodies disrupt the normal functions of the receptor by either:

→ uncontrollable activation or blocking receptor function

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8
Q

Describe haemolytic disease of the newborn

A

during birth, Rh+ fetal erythrocytes leak into maternal blood after chorion breaks
→maternal B cells are activated by Rh antigen and produce anti-Rh antibodies
→Rh antibody titre in mother’s blood
→Rh antibodies are small enough to cross the chorion and attach the foetal erythrocytes in second pregnancy

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9
Q

Describe Type 3 response

A

→IgG and soluble antigen form immune complexes eg complement which causes tissue damage

→activation of Fc-gammaR3 on mast cells induces their degranulation

→Immune complexes are cleared by phagocytes

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10
Q

Give examples of Type 3 response

A

→diptheria/tetanus vaccination

→antivenom

→farmer’s lungs

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11
Q

What is a difference between Type 2 and 3 reponse?

A

→Type 2= antigens are cell bound

→Type 3= antigens are soluble

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12
Q

Describe delayed-type hypersensitivity

A

→Th1 mediated response
→release IFN-gamma to activate macrophage
→production of chemokines, cytokines, cytotoxins

Th2 mediated:
soluble antigen
→Th2 activate eosinophil via IL-4,5, eotaxin
→production of enzymes and cytokines

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13
Q

Give examples of Th1 and Th2 mediated Type 4 reponse

A

→Th1= Tuberculin reaction

→Th2= Allergic contact
dermatitis

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14
Q

Give example of Type 4 reponse

A

→Mantoux test

→strong Th1 immune

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15
Q

Where does IgE bind?

A

→high affinity receptor of FcεR1 receptor on mast cells also oesoniphils

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16
Q

How do Bcells inform class switching?

A

→Th2 cells produce Il4 and IL13 which informs Bcell to switch to IgE

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17
Q

What might high dose exposure lead to?

A

→tolerance

18
Q

What are the features of inhaled allergens that promotes Th2 priming?

A 
→proteins- only proteins induce T-cell response
→enzymatically active
→low dose
→low molecular weight so can diffuse
→highly soluble
→stable
→binds to MHC-2
19
Q

What is filaggrin?

A

→links skin integrity and allergy

20
Q

What happens when filaggrin is defective?

A

→atopic dermatitis is greater

21
Q

Which protein may make dendritic cells pro-allergic?

A

→TSLP

→TH2 signalling molecule

22
Q

Describe mast cell activation

A

→antigen cross links bound IgE antibody, causing release of granule contents

→IgE produced upon first exposure

23
Q

What is early phase allergic response?

A

→mast cells

24
Q

What is late phase response mediated by?

A

→mediated by T cells
→recruit other cells by cytokine release

→Potentiate further responses

25
Q

What are some signs of acute allergic reponse?

A

→ Wheezing
→Urticaria
→ Sneezing,rhinorrhea
→ Conjunctivitis

26
Q

What are some signs of chronic allergic reactions?

A

→Further wheezing

→Sustained blockage
of the nose

→ Eczema

27
Q

What are the effector mediators produced by mast cells in early phase?

A

→histamine
→leukotrienes
→prostaglandins

28
Q

What are the functions of histamine in early phase?

A

→ increase vascular permeability

→ cause smooth muscle contraction

29
Q

What are the functions of leukotrienes?

A

→increase vascular permeability

→ cause smooth muscle contraction

→stimulates mucus secretion

30
Q

What are the functions of prostaglandins in early phase?

A

→chemoattractants for T cells,

eosinophils and basophils

31
Q

What are the cytokines released in late phase?

A

→IL-2 and IL-13
→promotes Th2
→promotes IgE

→TNF-alpha- promotes tissue inflammation

32
Q

What are the effects of mast cells in the GI tract?

A

→increased fluid secretion

→increased peristalsis- expulsion of GI tract contents

33
Q

What are the effects of mast cells on airways?

A

→decreased diameter

→increased mucus secretion

34
Q

What are the effects mast cells on blood vessels?

A

→increased blood flow

→increased permeability

35
Q

What do eosinophils express?

A

→express FceRI upon activation

36
Q

What are the effector functions of eosinophils?

A

→. Release highly toxic granule proteins and free radicals

→. Synthesise and release prostaglandins, leukotrienes and
cytokines

37
Q

What does late phase response depend on?

A

→allergen dose

→Continued synthesis and release of inflammatory mediators

38
Q

What does non-atopic asthma include?

A

→Occupational
→Exercise induced
→Nocturnal Asthma
→Post-bronchiolitic Wheeze

39
Q

What is chronic response in asthma caused by?

A 
→activation of 
 eosinophils, neutrophils, 
  T cells and other leukocytes
→cause airway 
  remodelling, permanent 
  narrowing of the airways, 
  and further tissue damage
→excess mucus
40
Q

What are some treatments for allergy?

A

→ inhibit effects of mediators on specific receptors
anti-histamine (block the histamine H1 receptor)

→inhibit mast cell degranulation
mast cell stabilizer (e.g. chromoglycate)

→ inhibit synthesis of specific mediators
 lipoxygenase inhibitors (e.g montelukast)
41
Q

What are other allergy treatments?

A

→Steroids – Act directly on DNA to increase transcription of anti-inflammatory mediators (e.g. IL-10) and decrease transcription of pro-inflammatory mediators (e.g prednisolone)

→Bronchodilators – Reverse acute effect of allergy on airways (e.g B2 agonist salbutamol), in acute phase

→Immunotherapy – Reverses the sensitisation to allergen by means of tolerising exposure

42
Q

Which cells do DCs present to in sensitisation?

A

→Th2 CD4 T cells and B cells

lolmyi (31 decks)

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