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Block 10 Week 4 > Mucosal Immunity - Hudig > Flashcards

Mucosal Immunity - Hudig Flashcards

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1
Q

in what mucosal organ does the response to pathogens start?

A

tonsils! they’re the first to see them

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2
Q

t/f: food molecules are often recognized as antigens

A

false! that’s how we can eat

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3
Q

What cells secrete mucus and mucins?

A

goblet cells

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4
Q

what is the function of commensal bacteria?

A

provide protection from harmful bacteria

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5
Q

t/f: commensal bacteria can be harmful if they become systemic

A

true

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6
Q

how much bacteria is present in the small intestine?

A

10^7 / ml

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7
Q

in what three IgA secreting areas are commensals not found?

A

eyes, breast, and lung

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8
Q

What cell type secretes b-defensins?

A

enterocytes

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9
Q

what cell type secretes a-defensins?

A

paneth cells

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10
Q

Describe how mucins and defensins work to kill bacteria?

A

mucins bind the defensins to the mucus layer and keep them from washing out. Defensins insert into the bacterial PM, create pores, and kill the bacteria

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11
Q

What cell “samples” the intestinal contents for bacteria and antigens?

A

M cells

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12
Q

what cells are inside the pocket created underside (basally) the M cell?

A

DCs, T and B cells

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13
Q

What is the predominant T cell type in the GI tract?

A

Tregs

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14
Q

A healthy GI tract has few T(blanks) and neutrophils

A

few TH17s and neutrophils

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15
Q

antigens that drain from intestinal villi and M cells can travel to which lymph nodes?

A

mesenteric

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16
Q

Mucosal B cells secrete what two types of Ig that are transported to the gut lumen?

A

IgM and IgA

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17
Q

Which Ig type is NOT found in the mucosa?

A

IgG`

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18
Q

Why do B cells pump IgA and M into the gut lumen?`

A
  1. directly anti-viral and antibacterial
  2. Abs aggregate pathogens and block their transport across the mucus
  3. block pathogen adhesion to epithelium
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19
Q

what percent of all lymphs are in the mucosa?

A

50%

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20
Q

how many grams of IgA are secreted per day?

A

3-4g

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21
Q

Intra-epithelial lymphoctyes are CD(blank)

A

CD8 T cells

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22
Q

What two specialized functions do the IELs have?

A
  1. standard CD8 mediated killing of virally infected cells

2. expression of NK cell receptor proteins to be able to kill non-specifically based on the presence of stress proteins

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23
Q

Describe the process of Ab formation from Ag presentation to an M cell

A
  1. M cell takes in Ag
  2. Ag presented to DC cell
  3. DC express Ag peptide via MHC II
  4. T cell activated from DC
  5. T cell travels to germinal center in Peyer’s patch and activates B cell
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24
Q

What regulatory cell responds in the mucosal system to DC displayed ags?

A

Tregs

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25
Q

What determines how Th0 cells differentiate in the gut?

A

The cytokine environment created by the DC cells

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26
Q

If Th0 cells become Tfh, what type of Ig is secreted from B cells?

A

IgA

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27
Q

If Th2 is the dominant differentiation, what IL do they release and what Ig does this induce?

A

Th2 releases IL 4 to make B cells to make IgE

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28
Q

What two cytokines do Tregs produce to shut down all T and B cell responses to ag?

A

IL10

TGF beta

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29
Q

t/f: Treg shut down of immune function is only seen in pathological conditions

A

false!! that’s what it should be, we want the gut to let everything just pass on through!

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30
Q

what are induced Tregs?

A

T regs activated by M cell activated DC cells

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31
Q

what antigens will induced Tregs recognize?

A

food and bacteria

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32
Q

Besides DC cells, what other cell secretes TGF beta to suppress the gut immunity?

A

enterocytes

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33
Q

The DC cells in the mucosa have what special CD marker on them?

A

CD103

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34
Q

t/f: IELs stay only withing mucosal tissues

A

true; they never see the spleen!

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35
Q

How does mucosal homing work?

A

binding of integrins to addressins to get lymphs into mucosal tissue from the blood then chemokines to attract them to the specific area

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36
Q

Where do you find addressins?

A

on the membranes of blood vessels and epithelium/enterocytes.

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37
Q

What addresssin is on high endothelial venules

A

MADCAM1

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38
Q

what addressin is on enterocytes?

A

E-cadherin

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39
Q

Where are integrins found?

A

on the surface of T cells activated in peyer’s patches or the mesenteric lymph nodes

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40
Q

Which integrin interacts with MADCAM1?

A

a4b7

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41
Q

Enterocytes/intestinal epithelia produce what chemokine to attract lymphs?

A

CCL25

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42
Q

What is the receptor on lymphs for CCL25?

A

CCR9

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43
Q

Which integrin binds to E-cadherin?

A

aEb7

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44
Q

What cell type expresses aEB7 and binds to E-cadherin?

A

IELs

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45
Q

everything except the IELs and the epithelial cells are found in what layer of the villus?

A

lamina propria

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46
Q

what Ig class do the granules of the mast cells contain in the LP of the villus?

A

IgE

47
Q

Thzero cells acted on by TGF0-beta and IL6 will differentiate into what cell type?

A

Th17

48
Q

Th1 cells are involved in (cytotoxicity/ADCC)

A

cell mediated cytotox

49
Q

Th2 cells are involvedin (cell mediated/ADCC)

A

ADCC

50
Q

Th17 cells recruit what cell type to the location?

A

neutrophils

51
Q

Are Tregs CD4 or CD8?

A

CD4

52
Q

what portion of the Ab structure is needed for the Ig to be transported into the gut lumen?

A

J chain

53
Q

Which two Abs have a J chain that allow them to be transported into the gut lumen?

A

IgA and IgM

54
Q

What is the molecule that binds to the J chain to allow Ig passage across the epithelial layer into the gut lumen?

A

plgR

55
Q

When IgA is released into the gut lumen, it is still attached to…

A

the secretory component of plgR

56
Q

IELs are CD4 or CD8?

A

CD8; they kill infected epithelial cells, that’s why theyre intraepithelial!

57
Q

In response to bacteria, memory Th17 cell secrete what cytokine?

A

IL17

58
Q

What is the target of IL17?

A

FIBROBLASTS; they then release chemokines to attract neutrophils

59
Q

which two chemokines do fibroblasts release to attract neutrophils?

A

CXCL2

CXCL8

60
Q

What affect could mAbs to IL17 receptors have?

A

useful in dz like RA where you want to limit neutrophil migration but overall disastrous to immune health in the gut

61
Q

t/f: celiac dz is different than wheat intolerance or wheat allergies

A

true; No auto-ab’s in wheat intolerance… No enteropathy to villi

62
Q

in the cases that are NOT classic Celiac, what are the two common findings?

A

malabsorption and

anemia

63
Q

what are the classical Sx of Celiac?

A

diarrhea
abd pain
failure to thrive
DAMAGED VILLI in small intestine

64
Q

What are the non-classical Sx of celiac?

A

delayed puberty
reduced growth
anemia
DAMAGED VILLI in small intestine

65
Q

What are the pathological changes to the villi in Celiac?

A
  1. villi are shortened
  2. cryptic hyperplasia
  3. > 25 IELs per 100 enterocytes
  4. Clinical Sx MUST occur at time of biopsy
66
Q

What type of anemia presents in celiac and why?

A

megaloblastic; failure to uptake B12-intrinsic factor complex

67
Q

what is the shortfall of using IgA auto-antibodies to tTG-2 to test for celiac?

A

person must have been exposed to gluten within the last two weeks

68
Q

What test for celiac has 100% specificity with a high negative predictive value?

A

serum IgA auto-Abs to EMA (endomysium antigens)

69
Q

Besides tTG-2 and EMA, what one other thing can patients develop IgA auto-Abs against in celiac?

A

IgA to de-amidated gliadin (gluten)

70
Q

What are the two most common HLA allelles in celiac?

A

90% DQ2
5% DQ8
last 5% positive for one alpha DQ2/8 and one beta DQ2/8 chain

71
Q

what is the caveat when doing a biopsy to determine celiac?

A

pts must have had gluten in the last two weeks for the biopsy to be positive

72
Q

how many sites are sampled in a celiac biopsy?

A

4

73
Q

How long does it take for symptoms to resolve once gluten has been removed from the diet?

A

months to years :(

74
Q

what is the half life of IgA in the serum?

A

6 days

75
Q

What is the characteristic malabsorption pattern seen in the mucosal folds of pt with celiac?

A

scalloping

76
Q

Describe the changes to the villi in celiac

A

villous atrophy and complete loss of villi

77
Q

How much gluten is needed to sustain/trigger the disease?

A

MICROGRAMS!!

78
Q

tTG2 modifies gluten to gliadin to fit into MHCII DQ2 and DQ8 which is then presented to what cell?

A

CD4 T cells

79
Q

T/F: the formation of autoantibodies are central in the formation of pathology in celiac

A

FALSE; no role! dz is caused by gluten directly stimulating T cells that damage small intestine architecture!

80
Q

how many IELs are seen per 100 enterocytes in celiac?

A

> 25

81
Q

Over activated IELs produced by activated anti-gliadin CD4 TH(blank) IELs kill enterocytes

A

TH1

82
Q

what extra set of receptors do CD8 IELs have in celiac?

A

NK cell receptors; they then kill enterocytes that are releasing stress signals

83
Q

what are the 2 T cell mucosal integrins and the one MALT chemokine receptor that are targets for mAb therapy in celiac?

A

t cell integrins: a4b7 and aEb7

chemokine: CCR9

84
Q

Refractory celiac disease may be due to (blank) spreading

A

epitope spreading

85
Q

(Crohns/UC) affects only the colon

A

UC

86
Q

(Crohns/UC) affects the ileum and the colon

A

Crohns

87
Q

(Crohns/UC) is associated with defensins

A

Crohns

88
Q

(Crohns/UC) is associated with mucins/mucus

A

UC

89
Q

(Crohns/UC) more often presents with abd pain and perianal disease

A

Crohns

90
Q

(Crohns/UC) tends to have GI bleeding

A

UC

91
Q

Cobblestoning of mucosa, and aphthous or linear ulcers are seen on endoscopy of…

A

Crohns

92
Q

Diffuse continuous involvement of the mucosa is seen on endoscopy of..

A

UC

93
Q

Fistulae, asymmetry, and ileal movement are seen on radiographs of…

A

Crohns

94
Q

Which dz shows mucosal discontinuity, transmural involvement, and granulomas?

A

Crohns

95
Q

Crypt abscesses and granulomas are only present in..

A

Crohns

96
Q

Loss of haustra and the formation of pseudopolyps are seen in (Crohns/UC)

A

UC

97
Q

Cobblestoning and fat wrapping are seen in…

A

(Crohns/UC)

98
Q

t/f: there is no HLA association in Crohns

A

true

99
Q

What is the monozygotic twin concordance in Crohns?

A

50%

100
Q

In Crohns, there is a genetic association with the variant of (blank) intracellular receptors and genes for autophagy

A

NOD2

101
Q

ileal Crohns is due to a lack of (a/b) defensins produced by Paneth cells

A

a-defensins

102
Q

colonic Crohns is due to a lack of b-defensins produced by the (blank) cells

A

enterocytes

103
Q

In Crohns, CD4 T cells differentiate into what two types predominately?

A

Th1 and Th17

104
Q

In what percent of cases of Crohns do we see granulomatous lesions

A

35%

105
Q

Studies indicate Tregs are (low/high) in Crohns

A

low; Tregs are used to dampen the immune response in the gut!

106
Q

What Ab drug can induce remission in crohns?

A

Rifaximin

107
Q

Anti-(blank cytokine) biologicals such as mAbs or decoy recepotors can reduce symptoms in Crohns

A

anti-TNFalpha

108
Q

Describe the overall process of T cell differentiation in Crohns

A
  1. Low levels of defensins
  2. More live bacterial ags presented in the lamina propria
  3. Activated APCs release profinflammatory cytokines
  4. Cytokines induces Th1 and Th17 and suppress Tregs
109
Q

What cytokine is released from mac’s and APCs to induce TH1?

A

IL12

110
Q

what cytokine is released from mac’s and APCs to induce Th17?

A

IL6
TGFb
IL1b
IL23

111
Q

How deep does the damage extend in UC?

A

to mucosa and submucosa only

112
Q

Which MUC transporters are low in UC?

A

secretory MUC2

transmembreane MUC3/4

113
Q

t/f: paneth cells and defensins are normal in UC

A

true

114
Q

Future therapies for UC include agonist ab to the (blank cyotkine) receptor made by Th2 cells which upregulates MUC5AC production

A

IL13

Block 10 Week 4 (9 decks)

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