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Immunology Test 2 > Immuno 16 > Flashcards

Immuno 16 Flashcards

1
Q

What is Type I Hypersensitivity?

A

IgE-dependent triggering of mast cells

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2
Q

What is Type II Hypersensitivity?

A

IgG antibody that is reactive with cell-surface or matrix antigens

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3
Q

What is Type III Hypersensitivity?

A

Involves production of antigen-antibody complexes

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4
Q

What is Type IV Hypersensitivity?

A

T cell-mediated hypersensitivity

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5
Q

What cells can induce class switching from IgM to IgE for Type I Hypersensitivity?

A

TH2 cells

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6
Q

What are allergens?

A

antigens that selectively stimulate TH2 cells that drive an IgE response

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7
Q

What are common properties of allergens?

A

Small proteins
Soluble
Carried on desiccated particles

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8
Q

In order to be a Type I Hypersensitivity, initial response must be what Ig response?

A

IgE

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9
Q

How do TH2 cells stimulate class switching to IgE?

A 
Effector TH2 cells deliver signals to favor class switching in B lymphocytes to IgE. Once the TCR of TH2 becomes ligated, TH2 CELLS: produce IL4,5,13
upregulated surface expression of CD40L and CD23 (low affinity receptor for IgE)
The combination of these signals induces class switching to IgE
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10
Q

Type I Hypersensitivity reactions are generally initiated by what cell?

A

Mast cells (with eosinophils and basophils involved)

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11
Q

What three cell types have IgE receptor FcgammaR1

A

Mast cells, eosinophils and basophils

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12
Q

How does IgE work in mast cells, eosinophils and basophils?

A

The IgE receptor becomes cross-linked by the antigen, which triggers the cell to degranulate, causing an inflammatory reaction

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13
Q

What are the two tests of testing an individual’s sensitivity to a particular allergen?

A

1st: injection of allergen to see a characteristic inflammatory reaction known as wheal and flare (appx 30 min duration)
2nd: 6-8 hrs post injxn, late phase rxn occurs at injxn site with widespread swelling, mediated by leukotrienes, chemokines and cytokines produced by mast cells following IgE-mediated activation

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14
Q

What is systemic anaphylaxis?

A

Wide-spread activation of mast cells degranulation causing both increase in vascular permeability and widespread constriction of smooth muscle. Caused by allergens in the blood.

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15
Q

What is anaphylaxis vs prophylaxis?

A

Anti-protection vs protection by the immune response. Basically fatal vs helpful

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16
Q

How can potential allergens be introduced directly to the blood?

A

Insect bite, drug injections, food or drugs that are rapidly absorbed

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17
Q

What is the most common cause of anaphylaxis?

A

IgE-mediated allergy to penicillin or other drugs (100 fatalities/yr)

18
Q

What is an anaphalactoid reaction?

A

Resembles anaphylaxis but no interaction between allergen and IgE.

19
Q

What is allergic rhinitis?

A

Hay fever, mild allergic response with violent bursts of sneezing and runny nose in response to inhaled allergens

20
Q

What is allergic asthma?

A

More serious that hay fever (allergic rhinitis), causing chronic breathing difficulties. Characterized by increased fluid into respiratory tract. Overall effect is trapping of air in lungs.

21
Q

Is chronic asthma a type IV hypersensitivity reaction?

A

YES

22
Q

What is urticaria?

A

Hives, caused by release of histamine by mast cells

23
Q

What is angioedema?

A

Inflammation caused by mast cell activation in deep subcu tissue. Swelling is more diffuse than urticaria.

24
Q

What are three strategies used to reduce the effects of allergic disease?

A
  1. Modification - of behavior and environment
  2. Pharmacological - drugs that reduce impace of contact with allergen (antihistamines, corticosteroids, cromolyn sulfate, epinephrine)
  3. Immunological - prevent production of IgE, shifting towards IgG response
25
Q

What are the effects of corticosteroids in allergic treatment?

A

Suppresses leukocyte function, used to treat chronic inflammation of asthma, eczema or rhinitis

26
Q

What are the effects of cromolyn sulfate in allergic responses?

A

Prophylactic inhalant, preventing degranulation of mast cells and granulocytes

27
Q

What is the mechanism of epinephrine in allergic treatment?

A

Stimulates reformation of tight junctions between endothelial cells, reducing the permeability of blood vessels, diminshing tissue swelling and raising BP. also relaxes, bronchial smooth muscle and stimulates the heart

28
Q

Why do people rarely develop allergic disease to parasite infections?

A

While a vast amount of IgE is produced in response, only a part of that is parasite-specific. The non-specific IgE outcompetes the parasite-specific for binding on mast cells,basophils and eosinophils. Prevents the parasite from triggering an IgE effector mechanism. Allows the parasite to evade immune response

29
Q

What is a side effect of living in an area that has high rates of parasitic infection?

A

Having low allergic reactions rates

30
Q

What is Type II Hypersensitivity?

A

Reactions caused by antibodies specific for altered components of human cells, mediated by IgG.

31
Q

What are examples of Type II hypersensitivity?

A

Penicillin, quinidine and methyldopa allergic reactions

32
Q

How does penicillin cause Type II hypersensitivity?

A

Penicillin causes new epitopes to be formed on cell surfaces that stimulate production of IgM and IgG antibody specific for the new epitope. Pencillin-modified RBCs must be coated with complement, facilitating phagocytosis by macrophages. Macrophages present the newly formed epitopes to CD4 T cells to produce Effector TH2 cells. These cells supply help to antigen-specific B cells. IgG Abs bind to altered RBCs a stimulate destruction by complement cascade or macrophages. End result is RBCs destroyed.

33
Q

What is Type III hypersensitivity?

A

Reactions caused by immune complexes (Ab-antigen) formed from IgG and soluble antigens

34
Q

How is treatment of large immune complexes different from small ones?

A

Large immune complexes are more efficiently taken up by macrophages, while small ones remain soluble and deposited along blood vessel walls.

35
Q

How does the accumulation of immune compexes lead to Type III hypersensitivity?

A

When sufficient immune comlexes accumulate, circulating leukocytes recognize the immune complexes thru the Fc and complement receptors, activating their inflammatory responses.

36
Q

What is serum sickness?

A

A type III hypersensitivity that is the result of IV administration of drugs used to treat a variety of illnesses. Caused by an accumulation of immune complexes. Characterized by chills, fever, rash, arthritis, vasculitis and sometimes glomerulonerphritsi

37
Q

What are two jobs that are often associated with type III hypersensitivity due to constant inhalation of antigens?

A

Farmers and Bird-Breeders

38
Q

What is Type IV Hypersensitivity?

A

Allergic reaction mediated by antigen-specific effector T cells.

39
Q

What is the other name for Type IV hypersensitivity?

A

Delayed-Type because they usually occur 1-3 days after contact with the antigen

40
Q

What are the most common causes of Type IV Hypersensitivity/

A

mycobacterial proteins, insect venoms, poison ivy, and small metal ions, and tuberculin

41
Q

What is the difference between poison ivy expose the first vs. subsequent times?

A

The first time results in the formation of immunological memory and effector T cells, due to the intracellular and extracellular mechanisms of the toxin.

The following times result in the typical visible response of rash and inflammation.

Immunology Test 2 (7 decks)

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