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CMD Block 2 > Lecture 16: Hypersensitivity Rxns > Flashcards

Lecture 16: Hypersensitivity Rxns Flashcards

1
Q

immediate type

A

Type I HS

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2
Q

immune complex

A

Type III HS

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3
Q

modified self

A

Type II HS

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4
Q

delayed type

A

Type IV HS

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5
Q

What Ab isotype mediates type I HS?

A

IgE

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6
Q

What Ab isotype mediates type II HS?

A

IgG

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7
Q

What Ab isotype mediates type III HS?

A

IgG

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8
Q

What Ab isotype mediates type IV HS?

A

not Ab mediated; it is T cell mediated

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9
Q

Describe the “priming” of a type I HS reaction.

A
  1. first exposure to Ag
  2. extraction of Ag across epithelium and taken up by APC
  3. Ag presented to CD4 T cell (NOT naive)
  4. Th2 activated
  5. Th2 secretes IL-4 (and activates B cell?)
  6. B cells diff into plasma cell
  7. plasma cell produces IgE
  8. IgE bound up by FcR on mast cell
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10
Q

What are some properties of antigens that promote the priming of Type I HS reaction?

A

Antigens that prime Th2:

  • proteins that bind MHC class II
  • allergens are often proteases
  • low dose
  • low molecular weight (to cross mucous membrane)
  • high solubility
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11
Q

T or F: you usually have a type I HS reaction the first time you are exposed to an Ag.

A

false: the system has to be primed –> you see rxn after the 2nd exposure

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12
Q

T or F: A TI-1 Ag can initiate a type I HS.

A

false: must be a T dependent Ag (Th2 mediates B cell production of IgE)

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13
Q

Once the immune system is primed, what initiates a type I HS reaction?

A

Ag has to crosslink 2 or more IgE on the surface of mast cells –> degranulation

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14
Q

How many IgE need to be crosslinked to cause a cause mast cell degranulation

A

2 or more

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15
Q

Where are mast cells found? How is this significant?

A

beneath epithelial layer –> Ag get to them quickly –> rapid degranulation after sys has been primed

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16
Q

T or F: The IgE that coat a single mast cell share the same exact specificity.

A

false: there are varient different specificities

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17
Q

What enzymes are found in mast cells and that are their fucntion?

A

trypase
chymase
cathespin G
carboxypeptidase

remodeling of connective tissue matric

18
Q

What are the toxic mediators in mast cells? What are their biological effects?

A

histamine and heparin

toxic to parasites
inc vascular permeability
causes smooth muscle contraction

19
Q

What is the major cytokine released by mast cells? What effect does it have?

A

TNF-a

  • promotes inflammation
  • stimulate cytokine production by many cell types
  • activates endothelium
20
Q

What is a wheal and flare reaction?

A

local degranulation of mast cells causing a hive (due to injection of Ag to test for specific hypersensitivity)

21
Q

What is urticaria?

A

a rash due to type I HS (all over body = systemic exposure)

22
Q

What does mast cell degranulation in the GI tract cause?

A

inc fluid secretion and peristalsis –> expulsion of GI tract contents (diarrhea, vomiting)

23
Q

What does mast cell degranulation in the airways cause?

A

decreased diameter and inc mucosal secretion –> expulsion of airway contents (phlegm, coughing)

24
Q

What does mast cell degranulation in the blood vessels cause?

A

inc blood flow and permeability –> edema, inflamm, inc lymph flor and carries Ag to lymph nodes (to prime T/B cell response –> anaphylactic shock)

25
Q

Ag in blood stream enters tissues and activates connective tissue mast cells throughout the body (is…)

A

anaphalaxis

26
Q

What affect does anaphylaxis have on the heart and vascular system?

A
  1. inc capillary permeabiluty
    • fluid enters tissues –> swelling/edema (including tongue)
  2. Loss of BP (from fluid loss)
  3. dec O2 to tissues
  4. irregular heartbeat
  5. anaphylactic shock
  6. loss of consciousness
27
Q

What is the effective treatment of anaphylaxis? Why?

A

epinephrine –> causes rebound of BP

28
Q

What are common allergens that elicit systemic anaphylaxis?

A

drugs
serum
venoms
peanuts

29
Q

What syndromes are IgE mediated?

A 
systemic anaphylaxis
wheal and flare
Hay fever
Bronchial Asthma
Food Allergy
30
Q

Describe the type II HS reaction.

A

(Penicillin-induced)
1. Penicillin binds RBCs and leukocytes
2. Self determinant on RBC changes
3. (for some people) self determinant is recognized as invader and complement is deposited
4. these complement laden RBCs are phagocytosed by macrophages
5. macrophages process these RBCs and load altered self peptides onto MHC class II
6. recognized by Th2 cells
7. Th2 activate B cells –> plasma cells
8. plasma cells secreted IgG which binds to penicillin-altered RBCs
9. activation of C1-C9 –> LYSIS
OR
Activation of C1-C3 –> phagocytosis of RBC-Ab immune complex by macrophage

31
Q

What gross change is associated with penicillin hypersensitivity reaction?

A

rash

32
Q

Describe type III HS.

A
  1. Ag injected into into a person with IgG Ab specific to it
  2. Immune complexes form with that Ag in tissue
  3. Complement activated
  4. C5a that results binds C5a-R on mast cell
  5. immune complex binds FcgRIII on mast cell
  6. Degranulation
  7. local inflammation, inc fluid and protein release, phagocytosis, and blood vessel occlusion (vasculitis, nephritis, arthritis)
33
Q

What organ is most susceptible to type II HS?

A

kidney

34
Q

How long does a type III HS reaction to present?

A

1-2 hrs after Ag exposure

35
Q

In a subcutaneous type III HS reaction, what is the name of the resulting disease and where are the immunocomplexes deposited?

A

Arthus Reaction on perivascular area

36
Q

What is “farmer’s lung”?

A

a type III HS reaction in which immune complexes are deposited in lung due to constant exposure to a mold in hay

37
Q

What are 2 type III HS immune complex diseases?

A

farmer’s lung and bird-Fancier disease

38
Q

Describe type IV HS.

A

(delayed hypersensitivity)
1. Ag is processed by tissue Ag and stimulates Th1 cells

  1. Th1 secrete:
    -chemokines -> macrophage recruitment
    -IFN-g -> activ macrophages, inc release of inflamm mediators
    -TNF-a and LT -> local tissue destruction; inc expression of
    adhesion molecules on blood vessels
    -IL-3 and GM-CSF -> monocyte production by BM
39
Q

Describe the tuberculin reaction.

A
  1. small amt of MTB protein injected sub-Q
  2. picked up and processed by macrophages
  3. Th1??? cell recognizes Ag and releases cytokines
  4. T cells, phagocytes, fluid, and protein move into sub-Q tissue
  5. look for inflamm response 24-72 hrs later
40
Q

How does poison ivy elicit a hypersensitivity response?

A

Pentadecatechol penetrates skin and covalently binds host proteins forming new, non-self Ag–> T cell spc tp Ag are produced

CMD Block 2 (38 decks)

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