Hypersensitivity

Question 1

How can identifying the antigen specificity of a T cell receptor help in determining if a T cell proliferation is neoplastic?

Answer 1

If they all have the same TCR then the proliferation is clonal and likely neoplastic

Question 2

So if we can use the TCR to identify a T cell neoplasm, what can be use to identify a B cell neoplasm?

Answer 2

immunoglobulins - if it’s all the same antibody, likely neoplastic

Question 3

What mediates a type 1 HSR?

Answer 3

It’s a rapid immunologic reaciton occuring within minutes of exposure, mediated by IgE-dependent activation of mast cells

Question 4

What leukocytes in particular are recruited in type 1 HSR?

Answer 4

eosinophils

Question 5

What does “atopy” refer to?

Answer 5

the predisposition to develop localized immediate hypersensitibity reactions - genetic

Question 6

Atopic individuals tend to have higher levels of what Ig in the serum?

Answer 6

IgE (and more IL-4 producing TH2 cells)

Question 7

The immediate reaction in Type 1 HSR is characterized by what?

Answer 7

vasodilation, congestion, and edema

Question 8

The late phase reaction in Type 1 HSR occurs when? Is characterized by what?

Answer 8

2-24 hours after the immediate reaction. characterized by an inflammatory infiltrate rich in eosinophils, neutrophils and T cells

Question 9

What are some examples of LOCALIZED allergic reactins?

Answer 9

1. allergic rhinitis
2. some forms of bronchial asthma
3. utricaria (hives) - but can also be systemic
4. allergic gastroenteritis (food allergy)

Question 10

What’s the tratment for localized allergic reactions?

Answer 10

avoid the allergen, antihistamines, corticosteroids, leukotriene modifiers, immunotherapy

Question 11

What is systemic anaphylaxis typically characterized by?

Answer 11

a life threatening systemic allergic reaction with bascular shock, widespread edema and difficulty breathing due to massive mast cell activation

Question 12

What are some common inciting agents for the systemic anaphylaxis reacitons?

Answer 12

beta lactam antibiotics like penicillin, cephalosporins, radiocontrast agents, foods like peanuts and seafood, insect toxin like bee stings and latex

Question 13

What’s the treatment for anaphylaxis?

Answer 13

intramuscular epinephrine

Question 14

Describe desensitization therapy for bee sting allergies?

Answer 14

Repeated injection of very small amounts of th evenom to cause the immune system to develop increasingly greater amounts of IgG antibodies that can bind to the venom before they bind to mast cells

Question 15

What mediates a type 2 HSR?

Answer 15

ANTIBODIES! They bind to the antigen and cause complement activation and phagocytosis - inflammation, etc.

Question 16

WHat are some examples of type 2 HSR?

Answer 16

autoimmune hemolytic anemia
pemphigus vulgaris
goodpasture syndrome
myasthenia gravis
grave's disease
insulin-resistant diabetes
pernicious anemia
thromobcytopenic purpura

Question 17

Describe goodpasture syndrome.

Answer 17

Antibodies attack a noncollagenous protein in the basement membranes of the kidney glomeruli and lung albeoli, so you get complement and Fc receptor-mediated inflammation leading to nephritis and lung hemorrhage

Question 18

What mediates a type 3 HSR?

Answer 18

antigen-antibody complexes that get stuck in blood vessels and elicit inflammation

Question 19

What are two areas in the body that are particulatly sensitive to type 3 HSR?

Answer 19

blood vessels and any organ where blood is filtered to form other fluids - like kidney sand synovium (so arthritis, vasculitis, and glomerulonephritis)

Question 20

Levels of what complement protein can be used to monitor type 3 HSR disease activity?

Answer 20

C3 - low levels indicate active disease because the classical pathway is in hyperdrive due to the ICs and you get depletion of C3

Question 21

What are some examples of diseases cause dy type 2 HSRs?

Answer 21

systemic lupus erythematosus
poststreptococcal flomerulonephritis
polyarteritis nodosa (hepatitive B!)
reactive arthritis (from bacterial infections)
serum sickness

Question 22

What mediates a type 4 HSR?

Answer 22

T cells!

Question 23

What are the two mechanisms of T-cell mediated hypersensitivity?

Answer 23

1. delayed-type hypersensitivity

2. T-cell mediated cytotoxicity

Question 24

Describe a delayed-type hypersensitivity reaction?

Answer 24

upon repeat exposure to the antigen, CD4+ T cells respond to antigen by secreting cytokines that stimulate inflammation and activate phagoytes, leading to tissue injury - this is the TB test!

Question 25

Describe a T-cell mediated cytotoxicity reaction.

Answer 25

The CD8+ T cells directly kill the tissue cells - like type 1 diabetes and graft rejection

Question 26

Describe the mechanism of granuloma formation.

Answer 26

It’s a type 4 HSR…
An antigen presenting cell presents the antigen to a CD4+ T cell
THe T cell then secretes cytokines to bring monocytes out of circulation into the tissue
The macrophages join together to form histiocytes and giant cells, in essence blocking off the invader

Question 27

When do granulomas form?

Answer 27

When there’s a persistent or nondegradable antigen like TB or fungi - also foriegn bodies

Question 28

What are some examples of type 4 HSR diseases?

Answer 28

Type 1 diabetes mellitus (against pancreatic islet cells)
multiple sclerosis (attacks myelin)
rheumatoid arthritis
crohn disease
peripheral neuropathy/guillain-barre?
contact dermatitis