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Microbiota On Mucosal > La2- Mucosal Immune System > Flashcards

La2- Mucosal Immune System Flashcards

1
Q

How are ilc non specific

A

No ag receptor

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2
Q

So how are they stimulated

A

Cytokines release by epi, mac, dc or dying cells

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3
Q

Give example of a parasite controlled by ilc2 response

A

Helminths

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4
Q

Give example of a leukocyte required in this process

A

Eosinophils (attracted by il5)

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5
Q

What are the 4 main roles of ilc

A

Link adaptive
Inflammation
Barrier function
Tissue remodelling/repair

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6
Q

What is the tuft cell- ilc2 loop for protists/helminths/ec

A

Stimulation of tuft cells like succinate produced by pathogen metabolism
Causes release of il25

Thsi stimulates ilc2 and release il13

Il13 able to skew differentiation into more tuft and goblet cells

Means efficient trapping in mucus barrier

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7
Q

Which intracellular protozoan killed efficiently by il12 induced cells ilc1,th1,NK

A

Toxoplasma gondii

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8
Q

How do cytokines signal for their development

A

Cytokine y chain receptor

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9
Q

Do they have the same tf like th1,2,17 induced by the cytokines

A

Yes

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10
Q

Which cytokines from ilc2 required for m2 development antiinflam

A

13,4

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11
Q

How does it induce healing (ilc2)

A

Through amphireglin (areg)

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12
Q

Which subset of ilc3 can present MHC for T cells

A

Ccr6+ ilc3

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13
Q

Other than amp increase what else does il22 do

A

Induced formation of tj (effective barrier eg claudin 2)
Induced amp exp and release
Induce mucin exp

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14
Q

Which type of ilc upreg in giardia lamblianinfection

A

Ilc3

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15
Q

What’s the diff between inductive and effector sites

A

Inductive is where ag uptake and presentation to naive cells occurs

Effector is where they migrate to for clearance eg from the circulation back to lp/subepithelium

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16
Q

Give 2 reasons microvilli exist

A

For sa for absorption or for sensing in tuft cells

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17
Q

What are tj for and made of

A

Keep cell polarity

Claudins, occludin, jams, zonulin

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18
Q

What other types of junctions are there cell to cell

A

Desmsoomes linking if together

Adheren junctions linking actin (made of cadherins )

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19
Q

What is there cell to basal Lamina

A

Hemidesmosomes and actin linked matrix junctions

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20
Q

What 3 trafficking occur in cells meaning polarity needed

A

Recycling back from endosome
Transcytosis
Degradation pathway (lysosome fusion)

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21
Q

What does the lymphoid lineage vs myeloid contain

A

B,t, NK and ilc

Myeloid is granulocytes and macrophages/dc/monocytes

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22
Q

What makes up the malt

A

Nalt- walldeyers ring (adenoids in nose and tonsils in mouth)

Balt- bronchus associated

Galt - lymphoid follicles and pp

No ugt

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23
Q

Give some unique features to mucosal immune system

A

M cells in nalt and galt
Siga
Constant active memory and T cells in absence of pathogen
Regulatory pathways/tolerance
Close contact with epithelium and the galt
Specific homing

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24
Q

Where do immune cells go from pp eg after ag presented

A

Draining to mesenteric Ln

Then through lymph to the circulation

Where via hev ag mucosal tissues can extravasate to their mucosal effector site

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25
Q

What adhesion molecule do hev at mucosal surfaces have for extravasation of lymphocytes

A

Madcam1 (bind integrins like a4:b7 or L-Selectins for naive)

(Lung tissue has pnad for l-selectin or vcam1 for a4:b1

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26
Q

How is balt diff to this

A

Has pnad or vcam1 instead

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27
Q

Which receptor marks lymphocytes mainly of si origin so they can home back via teck chemokine

A

Ccr9

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28
Q

What do iga+ plasma cells usually have (some T cells too)

A

Ccr10 (eg from nasal, salivary , mammary, intestine)

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29
Q

Where can they home to

A

Other mucosal sites like bronchi, mammary glands, large intestine

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30
Q

Through which chemokine at these sites

A

Mec

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31
Q

What marker for systemic homing do lymphocytes from nalt have (also naive before they are marked)

A

Ccr7 and L-selectin

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32
Q

Is homing established in ugt

A

No but evidence of systemic and mucosal immunity there

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33
Q

What does immunisation orally do

A

Mount Siga in gi tract , mammary and urt (salivary,lacrimal glands)

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34
Q

What does immunisation nasally do

A

Siga and igG at ugt and resp tract (lower and upper)

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35
Q

Do colons have isolated lymphoid follicles

A

Yes for some iga responses but local

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36
Q

Which receptor type in nasal immune cells are there for this response by vaccine

A

Ccr10 (so can migrate to resp tract which has mec)

37
Q

Give some ways ag can cross barrier

A

M cell transcytosis
Cross epithelial dc or macrophages
Through Apoptotic cells
Through goblet cells (if soluble)

38
Q

What do m cells have for recognition

A

Prion protein receptors

39
Q

What 2 types of cd8 cell are there

A

CD8 ab- for killing of infected cell

CD8 ydelta- killing stressed cells eg in the coeliac disease gluten response

40
Q

Which antibodies are specific to mucosal immunity

A

Polymeric

Dimeric iga
Pentameric igm

41
Q

Why are resp tract and ugt different

A

They have majority igG unlike the other mucosal with mainly iga

42
Q

How are iga / igm transported

A

Using pigr unidrectionally from baso lateral to apical side

Secreted with the sc via protease cleavage of pigr

43
Q

How is igG different

A

It is bidirectionally through fcrn receptor instead

Also can be exp on placental endothelial cells (for maternal blood to foetal blood transfer) not just epi cells

44
Q

Which disease associated with reduced iga specifically because of pigr polymorphism

A

Ibd

45
Q

What is seen in gf mice colonised for first time

A

Hypertrophic pp and increased Siga+ plasma cells

46
Q

Inducing which tlr causes coating of iga of Microbiota eg b and f

A

5 (induced th17 response and therefore iga release)

47
Q

How does il17 from th17 diff (by Microbiota) cause pigr exp

A

Il17 activates nfkb can cause pigr exp by binding an element in intron 1

48
Q

What else causes this nfkb binding

A

Tlr signalling in general through myd88 and activation of nfkb binding to pigr

49
Q

Mice Il-17r deficient caused what

A

Lower levels of pigr exp

50
Q

How else do Microbiota influence b cells/antibodies

A

Aid expression
And tslp sexretion from epi cells

51
Q

Give 4 roles of iga

A

Neutralise ag/ suppress motility of pathogens in lumen

Neutralise ag already endocytosed within endosome of epithelium

Export out using their pigr any toxins that crossed the epithelial barrier

Modulate innate immune responses

52
Q

How can they be anti inflammatory via innate modulation

A

Suppress complement activation

53
Q

What can they induce

A

Better phagocytosis eg of neutrophils or macrophages

Fcr stimulation on eosinophils for degranulation

54
Q

How do they interact with mucins to trap pathogens

A

Through cysteine residues

55
Q

What is the difference between classic and natural iga

A

Classic is T cell dependant activation and class witching high affinity fab region

Natural are present T cell independently and exhibit low affinity

56
Q

What cytokines help plasma cell and b cell survival and isotype switching in T cell independent (via dc)

A

April and baff

57
Q

What induced these cytokines in first place

A

Tslp (induced by Microbiota…)

58
Q

Explain t cell dep response for high affinity

A

First signal is via bcr and ag

Then second is via cd40-cd40l binding aswell as mhc on B-cell with tcr holding ag

= class switching and high affinity shm

59
Q

Can tlr stimulation also induce t-inde classswitching

A

Yes via nfkb signalling downstream to induce aid expression

60
Q

Natural iga can allow for tolerance how

A

Low affinity because probably reduced somatic hypermutation/activity

61
Q

Would pathogens induce shm

A

Yes likely through T cell responses better stimulation of macrophages

Eg cholera toxin

62
Q

What is the differences between iga1 and iga2

A

Iga1 has longer hinge region making it more flexible for cross linking
Also glycosylation via both o and n glycosylation

Iga2 shorter and only n glycosylation

Iga1 in majority of mucosal surfaces except colon where iga2 is more

63
Q

Why is n glycans present on the secretory component also important

A

Can bind bacteria instead of fab region

64
Q

Why would Colin need more iga2

A

More Microbiota and some have protease activity which can cleave epitopes of the longer hinge sequence of iga1 but can’t cleave iga2

65
Q

What happens for fcrn igG trafficking instead ef in lung or ugt especially in acidic ph from apical to baso lateral

A

Acidic ph apically causes recetor mediated endocytosis

Endosome trafficking
And then out by a transport vesicles where fcrn releases igG at neutral ph

66
Q

What can happen both ways in neutral ph

A

Pinocytosis and transcytosed and then released from fcrn in neutral ph

67
Q

What type of proteins are fcrn

A

MHC class 1

68
Q

In which disease is it upregulated unlikeniga

A

Ibd (because of adcc potentially and also complement activation = inflammatory )

69
Q

How many bacteria in colon

A

10^11 (the most)

70
Q

What would happen / happens in gf mice to immune system of mucosa

A

Reduced siga production and serum iga
Decreased T cell
Reduced cd8 cytotoxicity
Reduced lp size
Impaired rh17 responses

71
Q

Normally nfkb will cause inflammation via eg tlr system by microbes. Which butyrate induced molecule stops this system

A

Ppary

72
Q

How

A

Blocks it’s binding to genes and causes export out of nucleus

73
Q

Alternatively what can be done to block nfkb eg scfa do this (butyrate) and salmonella = tolerance

A

Block ikb degradation

74
Q

How can saa from sfb cause dc maturation

A

Gmcsf exp

75
Q

Which cytokines inducing ilc3 can non-disclosed / identified Microbiota induce release of by epi cells aswell as tslp

A

Il25 and 33

76
Q

How are ilc3 seen in Ibd crohns

A

Because gmcsf released blocks m2 development and induces more m1

= reduced antiinflam cytokines like tgfb which also needed for tissue repair

77
Q

Why is m1 bad

A

Can secrete proinflam like tnf, il23,il12, which can induce th1 and th17 responses = pro inflammatory and seen in Ibd

78
Q

Low affinity of natural IgAs can cause what

A

Binding to wide range of epitopes/microbes potential instead of highly specific

79
Q

Although Microbiota induced ilc3 which produces gmcsf can stimulate inflammatory m1, how can it also cause tolerance

A

Release of RA and IL10 (for treg differentiation)

80
Q

Which 3 malt sites have m cells for ag uptake

A

Tonsils, adenoids and pp

81
Q

How is PSA recognition by tlr2 example of tolerance

A

Induces cd4 cell release of il10 which is anti inflam

82
Q

Whcih 2 markers do naive lymphocytes have which allows their homing systemically to lymphoid tissues via HEV

A

Ccr7 and l-selectin

83
Q

What is the difference between cxr9 and 10

A

Ccr9 is majority only T cells and is specific to homing mainly in the small intestine via TECK chemokine released from those hev
Some b cells will have Ccr9 to home to si too but very little amount

Ccr10 is majority only b cells/iga plasma blasts from nalt, si,colon,stomach which then homes to diff mucosal sites like li, bronchi, mammary and salivary glands through MEC chemokine

84
Q

Dc will activate switching to the specific homing receptors eg Ccr9,10 a4:b7 or a1:b7. How

A

Retinoic acid release

85
Q

What does pnad and vcam1 bind in the bronchi

A

Pnad binds l-selection

Vcam bind a4:b1 integrin on some immunocytes eg from nalt

86
Q

Which markers instead are induced at the nalt which makes mucosal interact with systemic immunity

A

A4:b1 ine grin (binds vcam in bronchi)
Also systemic induction of Ccr7 and l-selectin (binds madcam) = systemic

87
Q

Why would gut immunisation not give immunity to airways

A

A4:b7 not important here

88
Q

What can iga - pathogenic or commensal complexes be recognised by which induces anti inflammatory il10 release vs downregulated inflam tnfa etc

A

Dc-sign expressing dendritic cells

89
Q

Give example where this has been shown

A

Shigella flexneri complexes (helps downregulate the inflammation)

Microbiota On Mucosal (22 decks)

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