L19 Flashcards Preview

Immunology > L19 > Flashcards

Flashcards in L19 Deck (29)
Loading flashcards...
1
Q

What is type 1 hypersensitivity?

A

↑IgE coats mast cells & basophils
Immediate response
Faster & larger response when +antigen

2
Q

How do you test for type 1 HST?

A

IgE skin test = patch/prick tests

RAST = measure allergen specific IgE in blood

3
Q

Because type 1 HST is a fast response, what is the pathophys that causes the delayed (late phase) response of this reaction?

A

Production of cytokines (AA metabolites)

Eosinophil response

4
Q

What is the difference between mast cells and basophils in a type 1 HST reaction?

A

Mast cells @ tissues

Basophils @ circulation

5
Q

What receptor does IgE bind? Explain how the receptor gets a response.

A

Fc epsilon

  • @ mast cells, basophils, eosinophils
    1. Receptors CROSS LINK
    2. Conformational change
    3. Lyn +P ITAM
    4. ITAM recruits Syk
    5. Release
  • Granules (immediate rxn)
  • Cytokines & AA metabolite secretion (late phase rxn)
6
Q

Is Fc epsilon signaling broad or specific?

A

Broad - binds the Fc region of IgE - doesn’t care which specific antigen is on the other end
Specific allergic reactions occur b/c of entry site - GI vs lungs vs. skin

7
Q

Walk through the normal pathway for IgE production and response.

A

Allergen binds B cell
B cell recruits Th2 (activated by innate response to allergen)
- Th2 promotes IgE isotype switching of B cell
B cell –> IgE plasma cell against that allergen
Secretes IgE
Bound IgE + mast cell
Mast cell release of granule products (immediate reaction) & cytokines (late phase reaction)

8
Q

Is IgE normally high or low [ ] in serum?

A

LOW
Moves into tissues to coat mast cells/basophils when not responding to allergen
How these cells get signals to pre-form granules so there can be an immediate response when an allergen presents

9
Q

What are the effects of immediate mast cell/basophil products vs late phase products?

A

All released at same time - different time frame of action
Immediate = vacular leak, broncho-constriction, GI motility
- Vasoactive amines: vasodilate & SM contraction
- Proteases: tissue damage
Late phase = tissue remodeling and inflam
- Cytokines: inflam, WBC recruit
- AA metabolites: vasodilate & SM contract

10
Q

Why might someone be predisposed to type 1 HST?

A

Genetics

  • Make more IgE for same antigen
  • Different cytokines to change Th2 differentiation (preferentially)
  • Mutations in Fcepsilon
11
Q

What is anaphylaxis? Mechanism, symptoms, treatment.

A
Mechanism = extreme type 1 HST
Symptoms:
- Bronchial constriction
- Edema
- CV collapse (hypotension)
Treat w/ EPI !!!!
12
Q

What are the anaphylatoxins?

A

C5a, C3a, C4a - inflam members of complement cascade
From MAST CELLS
↑SM contract
↑vasc perm

13
Q

What is bronchial asthma? What is the triad of symptoms?

A

Due to repeated type 1 HST rxns @ lung

  1. Periodic & reversible airway destruction
  2. Eosinophils –> chronic bronchial inflam
  3. Bronchial SM hypertrophy & hyper-reactive
14
Q

What are the 4 ways you can treat bronchial asthma?

A
  1. Cromolyn - stabilizes mast cells so don’t degran easily
  2. Leukotriene antagonists (phosphodiesterase inhibitors) block bronchial SM constrict
  3. Corticosteroids - ↓cytokines –> ↓inflam
  4. Epi (inhaler) broncho-dilator
15
Q

What is the idea of treating allergies via desensitization?

A
Slowly ↑allergen exposure in small doses
Make more IgG than IgE
IgG binds Fcgamma R2B receptor = inhibitory against B cells (can't make IgE)
May also see T2h tolerance - less class switching
16
Q

How are monoclonal Abs used for allergies?

A

= Abs against IgE

Neutralize & elim IgE

17
Q

Define an allergen.

A

= antigen that elicits type 1 HST rxn

18
Q

Define atopy.

A

Likelihood of a person to have an allergic response to something
Why you’re allergic to peanuts and I’m not

19
Q

What is type 2 HST?

A
IgM/G
2 = cy-2-toxic 
- Excess Ab --> complement & MAC
When bound @ cell surface - local tissue damage
More common in auto-immune
20
Q

What is type 3 HST?

A

IgM/G
Ab-antigen in CRICULATION deposit in BVs
- Defective CR1 b/c usually helps clear immune complexes from the blood
- Ab+antigen+complement –> MAC –> neutrophil attraction
Deposits happen in shared areas –> predictable symptoms

21
Q

What is goodpasture syndrome? What type of HST is it?

A

Auto-immune - type 2 HST
Ab against basement membrane (collagen)
@ Glomeruli –> nephritis and hematuria
- Fc receptor on glomerular membrane –> binds IgG –> inflammation and tissue destruction via complement
@ Lung alveoli –> lung hemorrhage & hemoptysis (coughing up blood)

22
Q

What is pemphigus vulgaris? What type of HST is it?

A

Type 2 HST
Ab against desmosomes in epidermal cell jxns
Form skin vesicles

23
Q

What is Graves disease? What type of HST is it?

A

Ab for TSH receptor
Stimulates receptor w/o hormone
Effects of hyperthyroidism (bulging eyes!!)

24
Q

What is Myasthenia Gravis? What type of HST is it?

A

T2 HST rxn
Ab binds ACh receptor @ NMJ –> no muscle contraction
Eyelid droop

25
Q

What are 2 type 2 HST diseases that could lead to anemia & bleeding?

A

B/c opsonization and phagocytosis due to Ab targeting

  • Autoimmune hemolytic anemia (lose RBCs)
  • Autoimmune thrombocytopenic purpura (lose platelets)
26
Q

Where are common deposit locations of Ab-antigen complexes in type 3 HST?

A

Where BVs branch!!!!
Kidney glomeruli
Joints

27
Q

What is an important examples of type 3 HST diseases?

A

Systemic lupus erythematosus (SLE) = Ab against DOUBLE STRANDED DNA

28
Q

What are 3 ways to treat chronic (type 2 & 3) HST diseases?

A
  1. Corticosterioids - limit inflam damage
  2. Plasmapheresis - remove bad Abs in blood
  3. IVIG - giving preformed IgG
    - Binds Fc gamma R2b = inhibits B cells switching
    - Bind IgE directly to ↑removal from body
    - ↓IL4
29
Q

Which receptor yields B cell inactivation (anti-inflam)?

A

CD32

Fc gamma R2B