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Flashcards in Hypersensitivity Deck (60):
1

What are hypersensitivities?

inappropriately vigorous host immune response to antigen

2

What are the four types of hypersensitivities?

Type I = anaphylaxis
Type II = Antibody-mediated cytotoxicity
Type III = Immune complex disease
Type IV = Delayed hypersensitivity

3

What is a type I hypersensitivity? How is it brought about?

Anaphylaxis - brought about by antigen binding to the surface of IgE-coated basophils or mast cells, causing release of histamine

4

How fast is a type I hypersensitivity?

Very fast

5

Seasonal allergies are what type of hypersensitivity?

Type I (IgE mediated)

6

What does it mean for an individual to be atopic?

those that have an increased tendency to develop allergies

7

IgE is mostly made to fend off against what type of antigen? What is its role in anaphylaxis?

Made for parasites, but released in response to allergens in atopic individuals

8

What is the default pathway in the absence of inflammation: Th1 or Th2? What is the significance of this in anaphylaxis?

Th2-- IgE production is the outcome of the lack of inflammation as seen in anaphylaxis

9

What is the "hygiene hypothesis"?

decreased exposure to pathogens early in life (which would favor the development of Th1-mediated immune responses), leading to the development of strong Th2-mediated immunity and subsequent IgE production

10

What are most respiratory allergens?

small molecules that are carried on larger particles such as pollen grains or mite feces

11

What sort of delivery method to the body do most respiratory allergens go through? What does this elicit?

Transmucosal delivery, causes Th2 IgE responses

12

Physiologic responses to parasites usually occur where?

Skin, airways, gut

13

What are basophils?

Granulocytes withgranules present in cytoplasm

14

Where are basophilis usually found?

Peripheral blood

15

Are basophils phagocytic?

Negative

16

How are basophils related to mast cells?

Similar, but arise from different cells

17

Where are mast cells usually located?

Near small blood vessels and post capillary venules in mucosal tissues

18

What is on the surface of mast cells that binds to IgE released during anaphylaxis? Binding to this area causes what?

Fc receptors--binding = histamine release and degranulation

19

How do anaphylatic reactions come about (what leads to hypersensitivity)?

1st exposure stimulates IgE production. Subsequent exposure to the allergen binds to the surface bound IgE and activates the cells to release their granule contents.

20

What are the two major chemicals in mast cells that mediate anaphylaxis?

Histamine, TNF-alpha

21

How does the amount of eosinophils in allergic individuals compare to that of non-allergy prone people?

Higher

22

What are the four major Leukotrienes, and what are their effects?

LTC4, LTD4, and LTE4.
Most potent substances known that cause smooth muscle contraction and increased vascula rpermeability

23

How long does it take leukotrienes to be synthesized? How do they compare to histamine?

Released more slowly than histamine, but have a longer effect

24

Where do eosinophils accumulate?

Nasal and bronchial mucosa in respiratory allergies, and in intestinal mucosa during certain worm infections

25

What is the function of eosinophils in the gut?

Attach to worms and release granules containing hydrolytic enzymes

26

When does the late response phase develop?

6-8 hours after immediate reaction

27

What are the chemicals that are released in the late phase response?

Prostrglandins
Leukotrienes
Chemokines
Cytokines

28

What is the cell type(s) responsible for the late phase response?

mast cells

29

What are the four events that occur in the late phase response?

1. 2nd phase muscle contraction
2. sustained edema
3. recruitment of eosinophils and Th2 cells
4. Remodeling of tossue

30

Eosinophils contain granules that have what?

hydrolytic enzymes that can be used to destroy certain parasites.

31

What synthesizes leukotrienes C4, D4 and E4?

Activated basophils and mast cells

32

What is the only treatment that can reverse anaphylaxis?

Epi

33

What is the mechanism of action of Epi?

binds to beta-adrenergi receptors to increase cAMP. This relaxes bronchial smooth muscles, tightens endothelial cell junctinos, and stimulates the heart

34

What is the mechanism of action of histamines?

Binds to histamine receptors to block further binding of histamine

35

What is the mechanism of action of Cromolyn sodium and theophylline?

block degranulation

36

What are the preventative treatments for anaphylaxis? How does it work?

Repeated treatments of anti-IgE. leads to development of Th1 cell mediated (IgG), downregulated Th2

37

What is type II hypersensitivity?

When antibodies bind to a cell surface to destroy it

38

What are the four types of antibody mediated reactions?

1. Complement
2. ADCC
3. Hemolytics disease of newborn
4. Non-cytotoxic reaction

39

What is involved in the complement mediated reactions of type II hypersensitivity?

Antibodies of the IgG or IgM classes activate the classical complement cascade, which is a sequentially activated series of proteins that can lyse cells. (e.g. blood transfusions)

40

What is involved in the ADCC mediated reactions of type II hypersensitivity?

Tumor cells or virus-infected cells are bound by IgG and are lysed by natural killer cells, monocytes or neutrophils via recognition through their Fc receptors.

41

What is involved in the hemolytic disease of the newborn reactions of type II hypersensitivity?

a mother makes IgG antibodies specific to the Rh blood group antigen expressed by the red blood cells of her child.

42

Are the IgG antibodies produced by the mother in hemolytic disease of newborns cytotoxic?

No, but antibodies coat RBCs, and these are destroyed = anemia

43

What is the treatment for erythroblastosis fetalis?

Anti-Rh antibodies given to mother bind to the fetal cells in the mother's circulation, causing their removal by spleen and liver phagocytic cells, thereby preventing sensitization of the mother's immune system

44

What type of hypersensitivity are Grave's disease and Myasthenia gravis?

Type II

45

What is the mechanism of action in Grave's disease?

Antibodies to the thyroid-stimulating hormone receptor cause the overproduction of thyroid hormones and the resulting hyperthyroidism

46

What is the mechanism of action in Myasthenia gavis?

antibodies to the acetylcholine receptor blocks nerve impulse transmission to muscles

47

What are the four ways immune complex diseases (Type III hypersensitivities) are induced?

1. Autoimmune diseases
2. Drug reactions
3. Infectious disease
4. Inhaled allergens

48

What is the pathogenesis of Type III hypersensitivities?

Formation of immune complexes, which lodge into tissues. Complement is then activated via classical pathway. C5a recruits lysosomal enzymes which release damaging enzymes to tissues

49

What is serum sickness?

Repeat injection of large amounts of foreign serum, causing immune complexes...

50

What normally removes the immune complexes? What chemical do these cells have that aid in this process? What happens to remove the immune complexes.

RBCs that bear complement receptor 1 protein (CR1), which binds C3b and C4b. These removed by liver

51

What happens to the RBCs in type III hypersensitivities that prevents them from removing complement?

Overwhelmed

52

What protein is present on the glomerulus that cause issues in type III hypersensitivities?

CR1 proteins that bind immune complexes

53

How long does it take to develop type IV hypersensitivity?

24-72 hours

54

PPD test for TB is an example of what type of hypersensitivity?

Type IV

55

What is the pathogenesis of Type IV hypersensitivites?

Small molecules complex with skin proteins, become internalized and expressed on class II MHC. CD4+ Th cells activated, lead to CTLs and interferon-gamma production.

56

When PPD is injected intradermally, macrophages present to T cells via class II MHC. What is the response of endothelial cells?

upregulate expression of vascular cell adhesion molecule-1 (VCAM-1)

57

What is the action of VCAM-1 in the PPD test?

alerts the circulating memory T cells that inflammation is occurring in the adjacent tissues and they bind and migrate into the tissues

58

When memory T cells have migrated to the PPD area, what happens?

Interferon gamma increaes macrophages. Tissue damage ensues, leading to positive test

59

Why don't PPD negative individuals develop immunity to the antigen?

Dose is too small to initiate primary immune response, and no memory cells generated.

60

What are granulomas?

Macrophages surroundsed by fibroblasts and CD4+ Th cells