IMM 1 gut immunity .... Flashcards

1
Q

Homeostasis in gut preserved by?

oral tolerance? depends on?

what promotes oral tolerance?

food allergy considered consequence of?

may underlie food allergen sensitization? where?

A
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2
Q

gut immunity

why is gut vulnerable?

what does this mean for the intestinal immune system?

A
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3
Q

exposures in early life, infant gut microbiota and future health?

early-life exposures?

symbiosis?

dysbiosis?

gut microbiota contrib to development of?

disruption causes?

A
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4
Q

microflora and GALT?

A
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5
Q

Microflora role in development GALT

GALT consists of?

What are ILFs what do they do?

Microbes and peyer’s patches

MAMPS stim what? also release of what?

A
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6
Q

immune response againse commensal microflora

how common commensal?

reside where?

can be killed by?

penetrate where? killed by?

survivors?

induce?

live bacteria and LNs

so how would B and T cells interact?

A
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7
Q

microflora health and disease

which cells associated with inflammation/Crohn’s?

Homeostasis?

allergy/food?

what do they release?

A
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8
Q

what comprise the mucosal firewall?

what does it do?

steps of microbes at the gut on?

A
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9
Q

relationship between microbiota, immune system, and diet

malnutrition affects?

microbiota acts as what barrier?

undernutrition?

recurrent infections predispose to?

A
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10
Q

SCFAs

come from?

these do what?

A
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11
Q

Immune tolerance?

oral tolerance?

failure results in?

A
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12
Q

central vs peripheral tolerance?

A
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13
Q

need for peripheral tolerance to antigens in intestine

why not central?

A
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14
Q

of critical importance in oral tolerance?

4 steps?

critical importance molecules do what?

A
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15
Q

tow main adverse food reactions?

non-toxic pathogenic mechanisms both?

Non-immune-mediated?

immune-mediated?

A
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16
Q

whats a food allergy?

two groups reactions?

IgE vs non-IgE?

delayed?

A
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17
Q

IgE associated appear when?

this is called?

first contact?

second?

A
18
Q

Relactivation of what cell is central in food energy?

releases what?

causes what?

(tryptase)?

A

release of mast-derived mediators such as histamine causes increase in vascular perm. and resulting exudation likely contains C3 and C5 (complement)

Tryptase from mast cells act on C3 and 5 to locally generate C3a and C5a which activate mast cells to further exacerbate the symptoms

19
Q

Treg cells and role in tolerance to allergens

A
20
Q

diet and environment on allergic sensitization

Vit D,A, folate?

high-fat?

gut microbiota

IgE?

microbiota suppress?

iTregs suppress?

A

increased Th2= allergy

21
Q

common food allergies?

most common?

3-5 years what happens?

into adulthood?

common but not severe?

A
22
Q

peanut allergy cascade?

A
23
Q

peanuts and nuts can contribute to what reaction?

by?

this stimulates?

which release? which increases?

A
24
Q

allergy tested?

A

skin prick (more sensitive)

blood test (test for IgE to specific food tested)

neither conclusive need also history to choose.

level of IgE doesn’t predict severity

gold standard is double blind oral food challenge

25
Q

systemic and local food allergy

A
26
Q

anaphylactic reactions

what type of reaction?

what is it?

result from what as a result of events mediated by what?

effects?

highly sensitive can have response to?

A

peanuts, tree nuts, seeds, seafood, spices, celery, eggs, mild and some fruit

27
Q

Non IgE mediated food allergy

(T-Cell mediated)

what type?

major tirggers?

what type of injury?

caused by what?

A

delayed up to 48 hours

28
Q

non IgE-mediated food allergy

(complement)

A
29
Q

cow’s milk allergy is what mediated?

high percentage show no what?

skin prick test?

in this situation what kind of hypersensitivity?

A
30
Q

Peanut allergy

mediated?

other than IgE what else?

A
31
Q

Food intolerance

is what?

other types?

A
32
Q

types of causes for food intolerance

A
33
Q

Celiac disease

predisposing factor?

mostly express?

these have what kind of response?

general population have this?

what else is involved?

hallmark of CD?

specifically associated with this disease?

stong link with?

A
34
Q

Ag processing and presentation?

MHC II

found on?

Ags taken up by?

protein Ags undergo?

loaded into?

Ag-free MHC expression?

A
35
Q

Gluten is what-rich?

digestion?

rich in what residues?

deamidated by? what is deaminated?

results in formation of?

Cd patients express?

A
  • proline-rich
  • poorly digested (lack of prolyl endopeptidases)
  • rich in glutamine res

peptides 10-50 formed left undigested

  • some of the gultamines damidated by tissue enzyme TG2
  • this results in formation of negatively charged glutamic acid residues
36
Q

Gluten

Gluten-specific Th() cells are generated

tissue damage occurs in what hypersensitivity?

release of what? development of.what?

autoantigen in CD?

B cells?

leads to?

A
37
Q

TG2 Abs isotypes?

assaying used in?

specificity?

previous diagnosis of CD needed?

A
38
Q

overview pathogenesis of celiac disease

gluten peptides resistant to?

what creates potent immunostimulatory epitopes?

presented via?

CD4 T cells secrete what? which inducces release of? by? resulting in?

Th2 drive production of?

what helps maintain Th1 response?

what links in innate immune response?

A
39
Q

Who to test (3)

how to test

recommended start?

no longer used?

what else?

confirm with?

A
40
Q

Genetic testing

All have CD associated with?

how much for each?

use test of these to do what?

A