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Gastrointestinal > wk 2 2 mucosal immunity > Flashcards

wk 2 2 mucosal immunity Flashcards

1
Q

physiological functions of mucosal tissues

A 
gas exchange 
food absorption 
sensory activities
reproduction 
#
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2
Q

glands which secrete mucosas

A 
lachrymal 
salivary
mammary
kidney
uro-genital tract
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3
Q

where would classic lymph nodes be located in GI

A

mesentery

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4
Q

distinctive anatomical featurees of gut mucosal immune system

A

intimate relaitonship betwen mucosal epithelia and lymphoid tissue
special structure
specialised mechanisms

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5
Q

effector mechanisms of gut mucosal immunity

A

activated/memory t cell predominate

‘natural’ effector/ regulatory T cells

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6
Q

immunoregulatory of gut mucosal cells is done by (2)

A

active down regulation of immune response

inhibitory maccrophages and tolerising dendritic cells

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7
Q

disease which causes constant inflammation of gut

A

chron’s disease

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8
Q

area of activationin gut immune cells

A

peyer’s patch

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9
Q

which are is covered by an epithelial layer containing specialised cells called M cells, tht have characteristic membrane ruffles (M= microvilli)

A

peyer’s patch

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10
Q

microvilli increases

A

surface area

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11
Q

where are dendritic cells located in peye’s patch

A

intimately close to M cell, directly behind

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12
Q

other than help from M cells, how can dendritic cells provide immune response

A

can do through lamina propria, extend across the layer to catch the antigen from the lumen of the gut

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13
Q

`cells located in gut epithelium

A 
CD4
dendritic cell 
CD8
macrophage
mast cell 
dendritic cell
IgA 
plasma celll
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14
Q

MADCAM-1 is a

A

molecular adresin

on epithelium

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15
Q

t/f MAdCAM is onyl found in gut

A

false

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16
Q

most abundant antibody in intestinal response

A

IgA (80%) - mostly IgA2
also dimeric

(IgM = 15%)
(IgG=5%) - most abundant in systemic

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17
Q

name of recdptor which allows binding of IgA to epithelial face and into luminal gut

A

poly-Ig receptor

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18
Q

3 ways IgA provides protection in gut

A

secreted to gut and neutralise pathogens and toxins
bind to pathogens internalsied in endosomes and neutralise
can export toxins from within lamina propria while being secreted

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19
Q

t/f IgM can replace IgA

A

true
poly-Ig can bind to dimerics, IgM also dimeric
not as good but works for those with immune defiency

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20
Q

outline the characteristics of special T cells of gut

A

expresses alphaE:Beta7 = anchoring to epithelium, does not move
activated
restricted antigen receptor

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21
Q

what happens when a virus infects mucosal epithelium cell

A

infected vell - displays viral peptide to CD8 IEL (MHC class I)

activated IEL kills infected epithelium by perforin/granzyme and Fas-dependent pathways

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22
Q

when epithelum cells undergo stress (infection, damage, toxic peptides) and express MIC-A and MIC-B, what happens

A

IEL T cells bind to MIC-A,B via NKG2D, activates, CD8alpha:alpha bind to TL, kills strssed cell via perforin/granzyme pathway

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23
Q

what happens in coeiliac disease

A

more death of epithelium cells than production

epithelium becomes flat, reduces absorption (surface area decreases)

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24
Q

define oral tolerance

A

default response too oral administration of prootein state of specific peripheral unresponsiveness

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25
Q

which responses require a mediated response the most in gut

A

T cell

IgE

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26
Q

t/f commensal organisms help cause hyperesponsiveness of mucosa

A

false

regulates local hyporesponsiveness

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27
Q

how are T cells mediated 2

A

anargy/deletion of T cells
generation of regulatory T cells

both immunosuppresive and induce B cells switching to IgA production

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28
Q

3 things which when present in commensal bacteria inhibit dendritic cell maturation

A

PGE2
TGF-beta
TSLP

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29
Q

define t cell anargy

A

tolerance mechanism in which the lymphocyte is inactivated following antigen encounter, yet remains alive in a hyporesponsiveness state

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30
Q

MAdCAM-1 is an adressin molecule, what is this

A

ligand receptor

31
Q

when would dendritic cells be activated in gut

A

if microorganisms penetrate epithelium

dxpress strong co-stimulatory ligands and induce CD4 T cells to differentiate into effector Th1 and Th2 cells

32
Q

what activates the NFkB pathway

A

intracellular sensors in epithelial cells (PRR)

33
Q

defensins are

A

anti-microbial peptides

34
Q

how does an infection develop

A

if some of the immune response cells are over taken, oesnt work properly and so infections able to spread

35
Q

naive CD4 T cells can activate into effector Th2 or Th1 cells, what does each produce and effect

A

Th2 - IL-13 produced, epithelial repair and mucus secretion

  • IL-5 produced, recruits/activates eosinophils, promotes IgA production
  • drive B cells to produce IgE (main immuno for parasites)

Th1- IL-3,IL-9 activates mast cells (histamine, TNFalpha, MMCP)

  • activates macrophages
  • activates B cells, produce IgG2a
36
Q

helminths infection is a

A

parasites infection

37
Q

which effector Th cell is appropriate fro helminths infection

A

Th2

th1 will lead to a chronic infection, IgG good at removing bacteria not parasites

38
Q

how does HIV infect

A

infects dendritic cells, expresses co-stimulation and moves to lymph nodes
finds more hosts, infects CD4T cells (activated) - these migrate to carry out effector functions, widespread dissemination

39
Q

primary immunodeficiency disorders present usually with

A

mucosal dysfunction

40
Q

t/f selective IgA defiency is only viral

A

false

only bacterial

41
Q

common variable immunodefiency is due to

A

failur to differentiiate into Ig secreting cells

  • low immunoglobulins (IgA ect)
  • bacterial infection
42
Q

CVID associated infections are

A

recurrent sinopulmonary and GI infections

43
Q

XLA (x-length agammaglobulinaemia) only affects males t/f

A

true

44
Q

when does XLA present, why

A

7/8months

immunoglobulin from mother (IgG, dimeric IgA) depletes, dont make their own

45
Q

what is the defect found in XLA

A

no b cells

agammaglobulinaemia

46
Q

associated conditions of CGD (Chronic Granulomatous Disease)

A

granulomas-pneumona, liver abscess, perianal abscess, skin abscess

47
Q

associated bacteria of CGD

A

staph aureus

48
Q

CGD is failure of

A

phagocyte respiratory burst

49
Q

how is CGD treated

A

bone marrow transplant

50
Q

Severe Combined Immunodefiency (SCID) appears

A

in first few weeks

51
Q

SCID is a profound defect in

A

t and b cell imunity

52
Q

associated conditions of SCID

A

oral candidiasis
chronic diarrhoea
interstitial pneumonotitis

53
Q

how is type 1 hypersensitivity initiated

A

crosslinking of allergen specific IgE on surface of mast cells with specific allergen

54
Q

triggers for anaphylaxis 3

A

venom
drugs
food
due to systemic arrival (IgE secreted by plasma)

55
Q

how does food cause anaphylaxis

A

undigested proteins absorbed across gut, enters vasculature

56
Q

why is avoidance key for allergens

A

every time allergen in presented to immune, stronger memory response

57
Q

coeliac disease is

A

hypersensitivity (non-allergic) to gluten

58
Q

treatment for coeliac

A

gluten-free diet

59
Q

gamma interferon from gluten specific t cell activat eepithelial cells which produe IL-15, what does this induce

A

proliferation and activation of IEL

intra-epithelial lymphocytes

60
Q

activation of IEL and T cells causes

A

death of epithelial cells

61
Q

characteristics of coeliac intestine

A 
gut flattens (lymphocytes/IELs kill epithelial quicker than they can be produced) 
lots of IELs along mucosal surface
loss of villi
62
Q

2 genes associated with coeliac disease

A

HLA-DQ2

HLA-DQ8

63
Q

associated antibody production of coeliac disease 3

A

anti-gliadin
anti-endomysal
anti-tissuue transglutaminase

64
Q

how is coeliac disease diagnosed in adults

A

adults - serology determines if they have anti-tissue transglutaminase
then biopsy

65
Q

what may cause a patient coeliac disease be misdiagnosed

A

if they are IgA deficient - wont product anti-tissue transglutaminase

66
Q

t/f b cells can present antigens in secondary response

A

true

67
Q

why is if there is no gluten, there is no antibody

A

b cell binds to gluten complex contsinign transglutminase
t cell binds and produces anti-gluten
b cells instead produces antibodies for transglutaminase

68
Q

characteristics of Crohn’s disease

A

focal and discontinuous inflammation with deep eroding fissures
also granulomas may be present

69
Q

t/f granulomas in ulcerative colits

A

false -

70
Q

where does ulceritive colitis begin

A

rectum, moves proximally and contiguously

71
Q

ulcerative colitis is due to

A

distortion of crypts with infiltration of monocytes/neutrophils and plasma cells

72
Q

t/f inflammation/ulceration of ulcertive colitis only affects surface of mucosa

A

true

73
Q

treatment for ulceritive colitis

A

non-specific anti-inflammaotry and immunosuppressive drugs
steroids/azathioprine/cyclosporin/methotrexate
anti-TNF alpha

Gastrointestinal (73 decks)

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