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Block 10 week 4 > Mucosal Immunity-Hudig > Flashcards

Mucosal Immunity-Hudig Flashcards

1
Q

In celiacs, you get a loss of (blank)

A

duodenal villi

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2
Q

What is GALT?

A

tonsils, stomach, small intestine and colon

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3
Q

What is waldeyers ring?

A

the tonsils, and adenoids form a ring of lymphoid tissue around the entrance of the gut and airway

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4
Q

Where do responses to pathogens and antigens start?

A

germinal follicles with T and B cells

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5
Q

what are the absorptive cells of the intestine?

A

enterocytes

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6
Q

Food peptides and lipid micelles are absorbed from the GI lumen and are carried via (blank) to the liver. Food molecules are rarely recognized as foreign antigens.

A

hepatic portal vein

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7
Q

(blank) secrete mucus into the lumen.

A

Goblet cells

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8
Q

WHere do we have the most commensal bacteria?

What do they do?

A

colon > small intestine

Provide protection from harmful bacteria

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9
Q

Commensal bacteria has pathogenic potential if bacteria becomes (blank)

A

systematic

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10
Q

Commensals are not found where in the body?

A

eyes, breast, lungs

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11
Q

What 2 things control bacteria?

A

mucus and defensins

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12
Q

(blank) cells secrete mucus to bind defensins
(blank) secrete beta-defensins
(blank) secrete alpha-defensins
(blank) kill bacteria

A

goblet cells
enterocytes
Paneth cells
Defensins

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13
Q

Alpha definins are also called (blank)

A

cryptidins

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14
Q

(blank) are any of the granular epithelial cells with large acidophilic nuclei occurring at the base of the crypts of Lieberkühn in the small intestine and appendix.

A

paneth

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15
Q

Which has more goble tcells, the colon or small intestine?

A

colon

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16
Q 
Defensins are (anionic/cationic)
Mucus is (anionic/cationic)
A

anionic

cationic

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17
Q

(blank) bind to mucus, are retained and concentrated to kill bacteria. THey protect the underlying cells from bacteria

A

Defensins

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18
Q

Alpha and beta definisins are (bank) molecules and insert into bacterial membanes to form (blank) and kill bacteria. THis has major potential for recominant therapy

A

amphipathic

pores

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19
Q

For (blank) immunity, both mucus and defensins are critical

A

innate`

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20
Q

Less than (blank) millimeters of mucus binds defensins, and bacteria, promotes bacterial killing, and is protective barrier

A

1

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21
Q

What is the adaptive mucosal immunity of healthy people in response to oral pathogens?

A
  • antigens detected by M cells
  • Dendritic cells and T and B cells in the M cell area get activated (peyers patches)
  • Make a lot of T-regs
  • memory cells are made
  • cytotoxic T ells kill stuff
  • Mucosal B cells secrete IgM and IgA-> kill pathogen
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22
Q

(blank)% of all lymphocytes are in the mucosa. (blank) of IgA are secreted per day

A

50%

3-4 grams

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23
Q

What are the organized lymphoid tissues of the gut?

A

Peyers patches (m cells are found here)

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24
Q

What are the 4 cell types of the gut epithelium?

A
  • entercoytes
  • IELS (intra-epithelial lymphocytes)
  • neuroendocrine cells
  • goblet cells
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25
Q

(bank) cells are located above Peyer’s patches to transport antigens

A

M cells

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26
Q

Peyers patches are covered by an epithelial layer containing specialized cells called (blank) which have characteristic membrane ruffle.

A

M cells

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27
Q

M cells are highly specialized for antigen transport and are named for their (blank)

A

microfolds

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28
Q

Can M cells take up large antigens?

A

yes, whole proteins and bacteria

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29
Q

M cells provide an inner pocket for the presentation of transported antigens. (blank) cells digest proteins and microbes to present antigens. What regulatory cells respond in mucosal system to DC antigen?

A

T cells

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30
Q

What four cells divide in response to antigens?

A

TH1, TH2, TH17, T regs

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31
Q

DCs determine how (Blank) cells differentiate into subsets.

A

TH0

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32
Q

If THzero cells go to T follicular helpers, you get (blank) from B cells

A

IgA

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33
Q

If TH2 dominant, high IL-4 may generate (blank) from B cells

A

IgE

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34
Q

(blank) normally produced in high numbers, secrete IL-10 and TGF beta to shut down all T and B responses to antigen

A

T reg

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35
Q

(Blank) in the healthy mucosa directs CD4 T cells into induced, antigen specific T regs.

A

TGF beta

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36
Q

The unifected mucosal environment is rich in (blank). What resleased this?

A

TGF beta

Entercoytes
CD103 Pos DCs

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37
Q

T cell specific for self antigen recognized in thymus becomes a (blank) regulatory T cell.

A

Natural regulatory T cell

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38
Q

T cell specific for self or commensal microbiota antigen recognized in presence of TGF-beta becomes a (blank)

A

induced regulatory T cell (T reg)

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39
Q

What molecules are selectively expressed in GI?

A

Chemokines
addressin
adhesion molecules

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40
Q

(blank) is when you have mucosal selective trafficing i.e selective up regulation of certain receptors and integrins.

A

Lymphocyte homing

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41
Q

What are the chemokines and adhesion molecules utilized in lymphocyte homing?

A

CCL25
MADCAM
E-cadherin

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42
Q

Memory (Blank) are CTLs ready to kill and elminate viruses.

A

CD8 IELs

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43
Q

When a virus infects mucosal epithelial cells-> infected cells display viral peptide to (blank) via MHC class (blank). Activated IEL kills infected epithelial cell by (blank) and (blank) pathways

A

CD8 IEL
perforin/granzyme
Fas-dependent pathways

44
Q

DC-derived cytokines direct (blank) differentiation

A

CD4 T cell

45
Q

What T cell will be produced if a DC releases TGF-beta?

What will these cells secrete?

A

T reg cells
-TGF-beta, IL-10

The immune system suppressors

46
Q

What T cell will be produced if a DC releases IL-6?

What will these cells secrete?

A

Tfh cells

IL-21, ICOS

47
Q

What T cell will be produced if a DC releases TGF-Beta and IL-6
What will these cells secrete?

A

Th17 cells

IL-6, IL-17

48
Q

What T cell will be produced if a DC releases IL-12 and IFN-gamma?
What will these cells secrete?

A

TH1 cells

IL-2, IFN-gamma

49
Q

What T cell will be produced if a DC releases IL-4?

What will these cells secrete?

A

TH2 cells

IL-4 and IL-5

50
Q

(blank) is abundant in a healthy mucosa and favors T reg generation. Bacterial and viral products affects DCs to produce different cytokines

A

TGF beta

51
Q

DC-derived (blank) drives Th1s to favor (blank) proliferation and arming.

A

IL-12

CTL

52
Q

“homed” plasma cells secrete (blank and blank) that is transported into GI lumen

A

IgM and IgA

53
Q

The secreted IgA (from homed plasma cells) will bind to receptors on (blank) face of epithelial cell and will be endocytes –> then you will get (blank) to the apical face of epithelial cell takes place and the (blank) dimer is released into the lumen

A

basolateral
transcytosis
IgA

54
Q

(blank and blank) are the only antibodies able to get into the lumen (no IgG)

IgA and IgM function by binding antigens in the lumen of the GI and prevent them from reaching to the epithelial cell layer and prevent adhesion.

A

IgA and IgM

55
Q

IgM also has (blank) chain and is transported. Some IgM and (blank) may go into blood

A

J

IgA

56
Q

(blank) cells and (blank) cells are in the epithelium waiting for a viral infection so they can attack

A

CD8 IEL killers

IgE loaded mast cells

57
Q

(blank) cells are ready in case of bacterial infection

A

Memory Th17 (+ fibroblasts and neutrophils)

58
Q

(blank) cells prevent responses to food antigens

A

memory T regs

59
Q

(blank) cells call in neutrophils

A

Ag-Activated Th17 cells

60
Q

Fibroblasts secrete what 3 things?

A

CXCL2 and CXCL8

Chemokines

61
Q

Certain drugs or monoclonal antibodies will bind IL-17 receptors and inhibit (blank) and thus inhibit (blank)

A

fibroblast activation

neutrophil recruitment.

62
Q

What are the effector mechanisms of the mucosal immune system?

A
  • activated/memory T cells predominate even in the absence of infection
  • multiple activated “natural” effector/regulatory T cells present
  • Secretory IgA antibodies
  • Presence of distinctive microbiota
63
Q

What is the immunoregulatory environment of the mucosal immune system?

A
  • active downreg of immune responses (e.g. to food and other innocuous antigens) predominates
  • inhibitory macrophages and tolerance-inducing dendritic cells
64
Q

What are the 3 diseases mediated by mucosal immunity?

A
  • celiac disease
  • chrons disease
  • ulcerative colitis
65
Q

celiac disase affects 1-2% of the population and occurs everywhere. What is the mortality rate? WHat causes this?

A

10-30%

immune mediated

66
Q

Who does celiac disease most commonly occur in?

A

children

50% cases are classic and other just have malabsorption and anemia

67
Q

When do you typically diagnose celiac’s disease?

A

4 yrs

68
Q

Is celiac’s treatable?

What are the classic symptoms?

What are the nonclassical symptoms?

A

yes! gluten free diet

  • diarrhea
  • abdominal pain
  • failure to thrive
  • damaged villi in small intestine
  • delayed puberty, reduced growth
  • anemia
  • other symptoms
  • damaged villi in small intestine
69
Q 
In celiacs disease, the villi are (blank). You have cryptic (blank).
Greater than (blank) IELs per 100 enterocytes.
A

shortened
hyperplasia
25

(clinical symptoms must occur at time of biopsy for pathology to be detectable)

70
Q

What is the classic pathology of celiac disease?

A
  • chronic diarrhea
  • weight loss
  • abdominal distention
  • malabsorption of nutrient (stunting of children)
  • malabsorption of iron
  • failure to absorb vit B12 intrinsic factor complexes (megablastic anemia)
71
Q

What is the test for celiac’s disease?
When will this test work?
Whats the exception to this test?

A

-Serum IgA auto-antibodies to tissue transglutaminase 2
(97% specific, 94% sensitive)

  • Person must have been recently exposed to gluten (last 2 wks) for positive test
  • 3% of patients genetically lack all IgA
72
Q

What are all the ways you can diagnose celiac’s?

A
  • Serum IgA tissue transglutaminas 2
  • Serum IgA auto-antibodies to EMA (endomysium antigens)
  • Serum IgA antibody to de-amidated gliadin (gluten peptide)
  • HLA DQ2 or DQ8 allele
  • Biopsy positive results essential
73
Q

If you do an endoscopy of a small intestine of a person with celiacs, what will you see?

A

scalloping and villous atrophy

74
Q

What is the therapy for celiac disease?

A

-gluten-free diet (no wheat, barley or rye)

75
Q

What is gluten?

A

alcohol soluble protein of wheat

76
Q

What are 3 essential cell types necessary to generate a CD8 T cell cytotoxic response?

A

Antigen-> CD4 T helper cell-> B cells-> CTLs

77
Q

Gluten is digested to (blank) and is enzymatically modified by tissue transglutaminase 2 (tTG2) glutamic acid and gets a (blank) charge.

A

gliadin

negative

78
Q

The negatively charged Glu fits only into (blank) and (Blank). Now APCs can present antigen

A

MHC II DQ2 and DQ8

79
Q

90% of patients with (blank) are positive for celiacs

5% of patients with (blank) are positive for celiacs

A

DQ2

DQ8

80
Q

When gluten is broken down to negatively charged Glu, it gets presented by MHC II on APCs and then activate (blank) and they will proliferate

A

CD4 T helper cells

81
Q

What is endomesium?

A

lines outside of individual muscle fibers

82
Q

What is the B cell response in celiacs?

A
  • Abs to gliadin
  • Abs to tTG2
  • Abs to EMA
83
Q

Pathologists find >(blank) IELs per 100 enterocytes

in celiac disease

A

25

84
Q

what is the current celiacs hypothesis?

Why do the villi shrinK?

A

over activated IELs produced by activated anti-gliadin CD4 TH1s, IELs become numerous and activated IELs kill enterocytes.
-As enterocytes die, the villi shrink and become dysfunctional

85
Q

In celiac disease, CD8 IELs also have (blank) receptors

A

NK

86
Q

Ordinary CD8 CTL engages antigen in (blank)

A

MHC 1

87
Q

CD4 gets hella up regulated due to gliadin antigen-> IEL’s induced to express (blank) receptors -> enterocytes present (blank and blank) stress receptors-> IEL’s (NK cell/ CD8 cells) kill stressed enterocytes

A

NK

MIC A and MIC B

88
Q

What are potential therapies for celiac disease?

A

mAbs to block either of 2 T cell mucosal integrins or a MALT chemokine receptor

89
Q

refractory celiacs disease is thought to maybe be due to (blank0

A

epitope spreading

90
Q

What part of the bowel is affected by Chrons disease?

What is it associated with?

A

ileum and colon

defects of defensins

91
Q

What part of the bowel is affected by Ulcerative Colitis?

What is it associated with?

A

Colon

defects of mucus

92
Q

Chron’s disease may have lower (blank) recruitment than warranted for protection

A

neutrophil

93
Q

Clinically, (blank) tends to present more frequently with abdominal pain and perianal disease, whereas (blank) is more often characterized by gastrointestinal bleeding.

A

Crohn’s disease

ulcerative colitis

94
Q

(blank) mucosa and aphthous or linear ulcers characterize the endoscopic appearance of Crohn’s disease. Ulcerative colitis presents with (blank) involvement of the mucosa.

A

Cobblestoning

diffuse continuous

95
Q

Radiographic studies of patients with Crohn’s disease characteristically show (blank x 3). In contrast, radiographic studies of patients with ulcerative colitis show continuous disease without fistulizing or ileal disease.

A

fistulae, asymmetry, and ileal involvement

96
Q

Pathologically, Crohn’s disease features mucosal discontinuity, (blank), and (blank), whereas ulcerative colitis does not.

Crypt abscesses and granulomas are present only in (blank)

A

transmural involvement
granulomas
Crohn’s disease

97
Q

Which disease has fat wrapping and thickened walls?

A

Chrons disease

98
Q

Which disease has ulceration and pseudopolyps, continually?

A

Ulcerative colitis

99
Q

In chrons you have low (Blank)

In UC you have low (blank)

A

defensins

mucins

100
Q

What is this:
Thickening, obstruction and fissures thorughout GI, small intestine involvement
Are there transmural lesions?

A

chrons disease

Yes!

101
Q

Is there an association with HLA with Chrons disease?
Is there concordance in monozygotic twins?
Genetic associations?

A 
NO
50%
Gene: 
-intracellular NOD2 sensors
-Autophagy gene variants
102
Q

There is an implication of lack of defensins in Chrons. (blank) in the ileum and (blank) in the colon

A

alpha-defensins (paneth cells)

beta-defensins (enterocytes)

103
Q

How do you treat Chron’s disease?

A

Rifaximin
Anti-TNF alpha biologicals
Increase T regs

104
Q

What is the pathogenesis of Chron’s disease?

A

Not enough defensins, so more bacterial antigens-> bigger lymphocyte response -> sad colon

105
Q

Ulcerative colitis is limited to the (Blank) and damage extends only to (Blank) and (blank)

A

colon

mucosa and submucosa and no deeper

106
Q

What is the major issue with UC?

A 
low mucus
(normal paneth cell defensins)
107
Q

What are the future immunotherapies for UC?

A

IL-13 stimulation to increase mucus secretion

Block 10 week 4 (10 decks)

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