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Unit 3 Micro and Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is Type I hypersensitivity?

A

Immediate (anaphylactic) hypersensitivity

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2
Q

What is Type I hypersensitivity mediated by?

A

IgE

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3
Q

What is a common name for type I sensitivity

A

allergies and atropic disorders

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4
Q

What are some examples of common antigens that are allergens?

A

Pollen, insect venom, foods, drugs, plant oils, metals

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5
Q

What cytokine is important in the IgE response of Type I hypersensitivity?

A

IL-4

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6
Q

Which T helper environment favors the development of allergies?

A

Th2

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7
Q

What do mast cells contain?

A

1- enzymes
2- toxic mediators that increase vascular permeability and cause SM contraction
3- cytokines (TNF alpha) that promote inflammation and stimulate other cytokine production
4- chemokines (CCL3) to promote the influx of monocytes and macrophages and neutrophils
5- lipid activators (leukotrienes) cause smooth muscle contraction and increase vascular permeability

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8
Q

Describe an Atopic individual:

A

Individuals genetically susceptible and generally have higher levels of IgE and eosinophils

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9
Q

What are chemokines?

A

to promote the influx of monocytes and macrophages and neutrophils

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10
Q

Describe the phases of a Type I reaction:

A

2 Phases:

  • immediate phase (action of pre-formed mediators)
  • late phase (cellular infiltration)
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11
Q

Does the first exposure to an allergen create a hypersensitivity reaction?

A

no

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12
Q

Describe the initial sensitization to allergens in Type I reactions

A

1- exposure to antigen
2- antigen activation of Th2 cells and stimulation of IgE class switching in B cells
3- production of IgE
4- IgE binds to mast cells

These mast cells are now sensitized because they have IgE bound to them

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13
Q

What happens when an antigen binds IgE on a mast cell?

A

Degranulation of mast cell

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14
Q

What causes the late phase reaction in Type I?

A

TNK alpha plays a big role

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15
Q

What is the Hygiene hypothesis?

A

Suggests that the incidence of alergies has doubled over the past 10-15 years possibly due to better and increased hygeine which has resulted in less exposure to pathogens, whiich skews immune responses to Th2 instead of Th1

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16
Q

How is Type I hypersensitivity treated?

A

1- avoidance of the allergen
2- use of drugs that reduce the symptoms (anti-histamines)
3- desensitization to allergen
4- allergic peptide vaccination

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17
Q

What is Type II hypersensitivity?

A

Antibody-mediated (Cytotoxic) Hypersensitivity

18
Q

When do Type II reactions occur?

A

after antibody is bound to cellular proteins

19
Q

What do bound antibodies initiate in Type II reactions?

A

inflammatory responses in tissue

20
Q

For type II reactions, why are antibodies made?

A

May be produced because cell proteins have been altered

21
Q

What other granulocytes are involved in Type I? When are they activated?

A

Eos and Baso. Degranulate after they are activated by the immune response.

22
Q

What is an example of a Type II reaction?

A

hemolytic anemia, where the production of anti-RBC antibodies can result in destruction of RBC. results in lysis or phagocytosis of RBCs because compliment is activated

happens in mis-matched blood transfusions

23
Q

How are Type II, Type III and Type IV treated?

A

1- avoidance of the antigen
2- reduction of the impact of the immune response to the antigen with non-steroidal and steroidal anti-inflammatory
3- reduction of the immune response in general or specifically
4- induction of regulation response (T regs)
5- blocking of the effector mechanisms or allergic response-cytokines, co-stimulatory molecules

24
Q

What granulocyte is important for making mucous?

A

Eosinophils

25
Q

When can chronic asthma occur? What is it mediated by?

A

in the presence of allergin and without the presence of allergin

it is mediated by cytokines and eosinophil products

26
Q

Describe allergic asthma:

A

1-allergin capture
2- crosslinking of IgE on the mast cells
3- degranulation and releasing mediators that cause changes
4- Th2 cells that produce IL-13 (mucous production)

27
Q

What is the immune reactant for Type II? And what does it do?

A

IgG. They fix compliment.

28
Q

Which reaction results in autoimmune diseases?

A

Type II (antibodies target cell surface receptors)

29
Q

What is Type III hypersensitivity?

A

Immune-complex mediated hypersensitivity

30
Q

What causes Type III?

A

The deposition of persistent immune complexes of IgG and soluble antigens that are compliment fixing

31
Q

What are the qualities of IC that determine their pathogenicity?

A 
1- size
2- isotype
3- valency
4- charge
5- ability to fix compliment
32
Q

Where are the common sites of IC deposition? And what does these sites determine

A

1- intravenous
2- subcutaneous
3- inhaled

These sites determine the clinical manifestation

33
Q

Genetic component to asthma?

A

MHC genes, TCR genes, Th1 and Th2 regulation, IL-4 (anything that accefts expresion of IL-4 can lead to a predisposition)

34
Q

Give three examples of Type III hypersensitivity

A

1- Serum sickness
2- post-streptococcal glomerulonephritis
3- arthus reaction

35
Q

Explain how serum sickness is Type III hypersensitivity?

A

Response occurse after the development of antibodies to large amounts of foreign protein

36
Q

What is Type IV Hypersensitivity?

A

Delayed (Cell mediated) hypersensitivity

37
Q

What is Type IV mediated by?

A

Antigen-specific Th1 cells

38
Q

When does Type IV occur?

A

1-3 days after exposure

39
Q

What are the commonalities between Types II- IV?

A

May occur in response to foreign antigen

Also when an individual’s immune system reacts against autologous (self) or modulated self antigens  autoimmunity.

Impacted by genetic susceptibility and environmental factors

40
Q

How much more antigen is needed for Type IV vs Type II?

A

Type IV needs 100-1000X more

41
Q

What are some examples of Type IV?

A

1- Delayed-type hypersensitivity
2- Contact hypersensitivity
3- Celiac disease

42
Q

What is the effector cell of Type III?

A

IgG

Unit 3 Micro and Immunology (25 decks)

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