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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
What adhesion molecule do hev at mucosal surfaces have for extravasation of lymphocytes
Madcam1 (bind integrins like a4:b7 or L-Selectins for naive) (Lung tissue has pnad for l-selectin or vcam1 for a4:b1
26
How is balt diff to this
Has pnad or vcam1 instead
27
Which receptor marks lymphocytes mainly of si origin so they can home back via teck chemokine
Ccr9
28
What do iga+ plasma cells usually have (some T cells too)
Ccr10 (eg from nasal, salivary , mammary, intestine)
29
Where can they home to
Other mucosal sites like bronchi, mammary glands, large intestine
30
Through which chemokine at these sites
Mec
31
What marker for systemic homing do lymphocytes from nalt have (also naive before they are marked)
Ccr7 and L-selectin
32
Is homing established in ugt
No but evidence of systemic and mucosal immunity there
33
What does immunisation orally do
Mount Siga in gi tract , mammary and urt (salivary,lacrimal glands)
34
What does immunisation nasally do
Siga and igG at ugt and resp tract (lower and upper)
35
Do colons have isolated lymphoid follicles
Yes for some iga responses but local
36
Which receptor type in nasal immune cells are there for this response by vaccine
Ccr10 (so can migrate to resp tract which has mec)
37
Give some ways ag can cross barrier
M cell transcytosis Cross epithelial dc or macrophages Through Apoptotic cells Through goblet cells (if soluble)
38
What do m cells have for recognition
Prion protein receptors
39
What 2 types of cd8 cell are there
CD8 ab- for killing of infected cell CD8 ydelta- killing stressed cells eg in the coeliac disease gluten response
40
Which antibodies are specific to mucosal immunity
Polymeric Dimeric iga Pentameric igm
41
Why are resp tract and ugt different
They have majority igG unlike the other mucosal with mainly iga
42
How are iga / igm transported
Using pigr unidrectionally from baso lateral to apical side Secreted with the sc via protease cleavage of pigr
43
How is igG different
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
Which disease associated with reduced iga specifically because of pigr polymorphism
Ibd
45
What is seen in gf mice colonised for first time
Hypertrophic pp and increased Siga+ plasma cells
46
Inducing which tlr causes coating of iga of Microbiota eg b and f
5 (induced th17 response and therefore iga release)
47
How does il17 from th17 diff (by Microbiota) cause pigr exp
Il17 activates nfkb can cause pigr exp by binding an element in intron 1
48
What else causes this nfkb binding
Tlr signalling in general through myd88 and activation of nfkb binding to pigr
49
Mice Il-17r deficient caused what
Lower levels of pigr exp
50
How else do Microbiota influence b cells/antibodies
Aid expression And tslp sexretion from epi cells
51
Give 4 roles of iga
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
How can they be anti inflammatory via innate modulation
Suppress complement activation
53
What can they induce
Better phagocytosis eg of neutrophils or macrophages Fcr stimulation on eosinophils for degranulation
54
How do they interact with mucins to trap pathogens
Through cysteine residues
55
What is the difference between classic and natural iga
Classic is T cell dependant activation and class witching high affinity fab region Natural are present T cell independently and exhibit low affinity
56
What cytokines help plasma cell and b cell survival and isotype switching in T cell independent (via dc)
April and baff
57
What induced these cytokines in first place
Tslp (induced by Microbiota…)
58
Explain t cell dep response for high affinity
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
Can tlr stimulation also induce t-inde classswitching
Yes via nfkb signalling downstream to induce aid expression
60
Natural iga can allow for tolerance how
Low affinity because probably reduced somatic hypermutation/activity
61
Would pathogens induce shm
Yes likely through T cell responses better stimulation of macrophages Eg cholera toxin
62
What is the differences between iga1 and iga2
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
Why is n glycans present on the secretory component also important
Can bind bacteria instead of fab region
64
Why would Colin need more iga2
More Microbiota and some have protease activity which can cleave epitopes of the longer hinge sequence of iga1 but can’t cleave iga2
65
What happens for fcrn igG trafficking instead ef in lung or ugt especially in acidic ph from apical to baso lateral
Acidic ph apically causes recetor mediated endocytosis Endosome trafficking And then out by a transport vesicles where fcrn releases igG at neutral ph
66
What can happen both ways in neutral ph
Pinocytosis and transcytosed and then released from fcrn in neutral ph
67
What type of proteins are fcrn
MHC class 1
68
In which disease is it upregulated unlikeniga
Ibd (because of adcc potentially and also complement activation = inflammatory )
69
How many bacteria in colon
10^11 (the most)
70
What would happen / happens in gf mice to immune system of mucosa
Reduced siga production and serum iga Decreased T cell Reduced cd8 cytotoxicity Reduced lp size Impaired rh17 responses
71
Normally nfkb will cause inflammation via eg tlr system by microbes. Which butyrate induced molecule stops this system
Ppary
72
How
Blocks it’s binding to genes and causes export out of nucleus
73
Alternatively what can be done to block nfkb eg scfa do this (butyrate) and salmonella = tolerance
Block ikb degradation
74
How can saa from sfb cause dc maturation
Gmcsf exp
75
Which cytokines inducing ilc3 can non-disclosed / identified Microbiota induce release of by epi cells aswell as tslp
Il25 and 33
76
How are ilc3 seen in Ibd crohns
Because gmcsf released blocks m2 development and induces more m1 = reduced antiinflam cytokines like tgfb which also needed for tissue repair
77
Why is m1 bad
Can secrete proinflam like tnf, il23,il12, which can induce th1 and th17 responses = pro inflammatory and seen in Ibd
78
Low affinity of natural IgAs can cause what
Binding to wide range of epitopes/microbes potential instead of highly specific
79
Although Microbiota induced ilc3 which produces gmcsf can stimulate inflammatory m1, how can it also cause tolerance
Release of RA and IL10 (for treg differentiation)
80
Which 3 malt sites have m cells for ag uptake
Tonsils, adenoids and pp
81
How is PSA recognition by tlr2 example of tolerance
Induces cd4 cell release of il10 which is anti inflam
82
Whcih 2 markers do naive lymphocytes have which allows their homing systemically to lymphoid tissues via HEV
Ccr7 and l-selectin
83
What is the difference between cxr9 and 10
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
Dc will activate switching to the specific homing receptors eg Ccr9,10 a4:b7 or a1:b7. How
Retinoic acid release
85
What does pnad and vcam1 bind in the bronchi
Pnad binds l-selection Vcam bind a4:b1 integrin on some immunocytes eg from nalt
86
Which markers instead are induced at the nalt which makes mucosal interact with systemic immunity
A4:b1 ine grin (binds vcam in bronchi) Also systemic induction of Ccr7 and l-selectin (binds madcam) = systemic
87
Why would gut immunisation not give immunity to airways
A4:b7 not important here
88
What can iga - pathogenic or commensal complexes be recognised by which induces anti inflammatory il10 release vs downregulated inflam tnfa etc
Dc-sign expressing dendritic cells
89
Give example where this has been shown
Shigella flexneri complexes (helps downregulate the inflammation)

Microbiota On Mucosal (22 decks)

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