Flashcards in Immuno - Resp Deck (83):
What is a type I hypersensitivity?
immediate with IgE, mast cells and lipid mediators
What is a type IV hypersensitivity?
delayed, CD4 mediated
What is Atopy? or an atopic individual? 3 things are high?
IL-4 secreting TH2 cells
Will you know you're being sensitized to an allergen?
Not necessarily, you may not even realize until next exposure
example of a local response to Type I hypersensitivity?
Example of a systemic response to Type I hypersensitivity?
Responses to Type I hypersensitivity?
Immediate and late phase
are inhaled allergens lipids? sacharrides? or proteins?
protein via small carrier particles
are allergens usually insoluble?
You need high dose of allergen to be sensitized?
Only very low dose, like 1micro-gram per year
allergens are often proteins? enzymes? lipids?
What's Der p 1?
dust mite faeces allergen
T/F? DCs produce IL-4
Nope. They produce IL-33
What its the role of Basophils in Type 1 hypersensitivity?
Act as an APC
secrete IL-4 either after IL-33 or allergen binding
What do you need for TH2 differentiation?
1. CD40 antigen binding
3. IL-4 cytokine
Where are mast cells usually located?
mucosal/epithelial/near blood vessels
Mast cells bind IgE using what?
high affinity FcER
What's so special about FcER on mast cells?
The only one that can bind the antibody WITHOUT it's antigen...
3 steps for mast cell activation
1. secretion of preformed mediators (histamines)
2. synthesis and secretion of lipid mediators (protaglandins/leukotrienes)
3. cytokine production (slow)
initial (0-5min) wheal and flare is soft or hard feeling?
late phase (8-12 hours) mast cell activation is soft or hard feeling?
hard feeling due to mediators
Allergic response is dependent on what?
Type of tissue
Where and when are eosinophils usually found?
mucosal linings, found late in allergic response
What increases Eosinophil production in bone marrow?
IL-5 by TH2 and mast cells
What are eotaxins?
mediators that attract eosinophils to inflammatory site
increased sensitivity happens how on mast cells?
more FcEr on surface and IgE binding
4 treatments for allergy?
1. adrenaline (anaphylaxis)
2. B2 adrenergic receptor agonists (asthma)
What does T-cell desensitization/immunotherapy tolerance mean? 4 things
deviation of cytokines
decreased allergen-induced proliferation
What kind of hypersensitivity involved T-cells/macrophages and CD8 cells?
Why do you get Type IV hypersensitivity?
persistent antigenic stimulation
What is DTH?
Delayed type hypersensitivity
What happens in Delayed type hypersensitivity sensitization phase?
proliferation of TH1, helper T-cells, CD8 in lymph node, they go back to tissue and persist just waiting for next exposure
celiac disease have in common?
All are Type IV Delayed type hypersensitivity
Mycobacterium TB is a what kind of pathogen?
facultative intracellular pathogen
What's the good news with DTH and TB?
restrict 90% of growth
What's the bad news with DTH and TB?
small % of ppl interrupts respiratory function
What's a telltale sign of TB infection in lung tissue on microscope?
Granuloma: multinucleate giant cells epithelioid cells, lymphocytes
>90% of celiac disease ppl are what positive?
What does the Delayed type hypersensitivity do to the small intestine?
What's the incidence of celiac disease?
1 in 70
Normally, does gliadin peptides bind to HLA DQ2?
How does glutamine --> glutamate?
via tissue transglutaminase 2 (tTg2)
what's an autacoid?
4 things autacoids can do?
smooth muscle tone
What is Cysteinyl
a Leukotriene in allergies
What's red man syndrome?
allergic reaction to morphine or vancomycin
What is a possible reason behind exercise induced bronchospasm?
increased air flow through bronchi created hypo-osmotic surface enough to trigger mast cells
ITAMS have no what?
intrgral kinase activity
Diacylglycerol protein kinase C + inositol triphosphate Ca2+ mobilisation = ??????
degranulation of mast cells
Once IgE is bound, it activates MAPK which does what?
cytokine gene transcription
Once IgE is bound, it activates phospholipase C which does what?
How long does it take to cause mast cell degranulation?
When does mast cell activity peak?
4 immediate mast cell communication methods?
2 rapid mast cell communication methods?
3 slow mast cell communication methods?
Why are antihistamines not used in asthma?
older antihistamines were H1 receptor blockers however H1 activation will cause bronchospasm/constriction
What does histamine do to H2 receptors? 2 things
1. positive inotropic and chronotropic
2. Gastric acid secretion
H1 receptor activated by histamines does 6 things:
CNS - wakefulness
Should you block prostaglandins or cysteinyl leukotrienes? Why?
Leukotrienes cause it will only affect inflammation unlike prostaglandins which have lots of other effects
What's 5-lipoxygenase? how activated?
the inflammation bitch. It's all it does.
Activated by increased intracellular calcium
Where does the leukotriene receptor antagonists block LTs?
At CysLT1 receptor
What leukotriene attracts leukocytes?
Where does Aspirin, NSAIDS Coxibs act on?
What does phospholipase A2 do?
turns acyl lipid into Arachidonic acid
Cytokines are slow, what are they doing? 3 things
inducing gene expression changes
inflammatory cell infiltration
Which cytokines are highly regulated by glucocorticoids?
Which cytokines are not regulated by glucocorticoids?
3 things in the body that can inhibit mast cells?
What do the older mast cell inhibitors like disodium cromoglycate and nedocromil sodium cause release of?
Annexin-1 which resolves inflammation
What's the cons of disodium cromoglycate and nedocromil sodium
topical and local effects only
What is omalizumab?
expensive biologic: monoclonal antibody (Anti-human IgE antibody) that binds and prevents IgE to alpha chain of FcER1
Can you use omalizumab in asthma?
jury's still out on that one
I have asthma, I might take some NSAIDS/COX-2 inhibitors, cool?
NO. NO. NO. doesn't do shit in asthma or hay fever, it might provoke symptoms.
Crap Doc, I took aspirin for my asthma and it's getting worse! what do I do?!
I'll give you LTRA (leukotriene receptor antagonists)
What do glucocorticoids do?
inhibit mediator (cytokine) production in airways
When would you use an H1 receptor antagonist for allergies? 6 things
When would you NOT use H1 receptor antagonist?
Asthma or colds
3 classes of H1 receptor antagonists
1. sedative (chlorpheniramine, promethazine)
2. non sedative but risk of ventricular arrhythmia
3. newer nonsedative (cetirizine, loratidine)