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Gastro > Mucosal Immunology > Flashcards

Mucosal Immunology Flashcards

1
Q

What is the name of the specific immune follicles in the Large intestine?

A

Lymphoid follicles

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2
Q

WHat is the name of the specific area related to immunity in the small intestine?

A

Peyer’s Patch

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3
Q

What is concentrated in muscosal sites?

A

Specialised lymphoid tissue

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4
Q

Why is the immune system highly vulnerable to infection

A

Due to the fragility and permeability of the tract. Any food we ingest could be contaminated and require an immune response to remove the antigen

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5
Q

What 5 types of cells are found in the monolayer separating the microbiota from the lamina propria

A 
Enteroabsorptive cell
goblet cells 
neuroendocrine cells
paneth cells 
M cells
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6
Q

What is the benefit of the villi and crypts

A

THey provide a large surface area for antigens to interact

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7
Q

What is the purpose of the Paneth cells

A

They are defensins

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8
Q

What occurs in the Peyer’s Patches?

A

Antigen sampling and immune activation

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9
Q

What types of cells is the large intestine mostly made up of?

A

Crypts (not villi), enterocytes and lots of goblet cells and mucus

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10
Q

Which has the higher bacterial load? the small or large intestine

A

Large intestine

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11
Q

Why do enterocytes have a much more important contribution to antimicrobial peptide production in the large intestine?

A

There are no Paneth cells in the large intestine

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12
Q

Where do natural killer T cells have a more significant role to play?

A

In the colon

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13
Q

What are the main secretors of antimicrobial peptides

A

The Paneth Cells

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14
Q

What 3 types of cells capture, initiate the local immune response and carry out effector functions to clear any infection?

A

Intestinal epithelial associated - innate immunity, antigen capture and effector function
Peyer’s patches and lymphoid follicles - antigen capture and initiation
Lamina propria - effector cells (remove the danger and repair any damage)

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15
Q

How do dendritic cells capture antigens across the epithelium?

A

They can extend their processes to capture antigens from the lumen of the gut

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16
Q

What are the direct antigen sampling organisms of the gut?

A

The Peyer’s patches

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17
Q

Describe the structure of Peyers patchs

A

covered by an epithelial layer containing specialised cells (M cells) which have characteristic membrane ruffles

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18
Q

What is situated directly below an M Cell?

A

Dendritic cells

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19
Q

Describe the steps of the M cells

A

Uptake of antigen by endocytosis and phagocytosis
Transporation of antigen across the M cells in vesicles released at the basal surface
Antigen is bound to dendritic cells, activating T cells

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20
Q

What is the major effector molecule in the gut called?

A

IgA

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21
Q

What type of cells enter the Peyer’s patches form blood vessels?

A

T cells

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22
Q

What happens to the T cells in the Peyer’s patch when an antigen is transported across M cells?

A

They become activated by dendritic cells

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23
Q

What is the make up of the humoral intstinal response?

A

80% IgA
15% IgM
5% IgG

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24
Q

As peristalsis occurs, what happens to IgA

A

It is moving and being produced continuously

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25
Q

How does IgA move accross the membrane from the lamina propria to the lumen?

A

Endocytosis then transcytosis

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26
Q

What is the function of IgA cells

A

They bind and neutralise pathogens and toxins to prevent damage to the epithelial cells

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27
Q

What 3 ways can IgA work>

A

Bind to the antigen in the gut or on the mucus layer
Neutralise antigens in endosomes
Export toxxins and pathogens from the lamina propria whilst being secreted

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28
Q

What molecule takes over this role in patients who are IgA deficient?

A

IgM

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29
Q

How frequently are intraepithelial lymphocytes found?

A

1 in every 10 epithelial cells

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30
Q

What anchors intraepithelial lymphocytes in the epithelium

A

Expression of Alpha E: Beta 7 integrin

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31
Q

What is the main function of intraepithelial lymphocytes?

A

To kill infected epithelial cells by initiating programmed cell death

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32
Q

What are the 2 types of intraepithelial lymphocytes?

A

Virus speciic recognition - TCR/CD8 cells

Stress specific recognition - NK cells

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33
Q

How do TCR/CD8 cells kill?

A

Via FAS=FASLigand

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34
Q

How do NK cells kill?

A

Via perforin/granzyme system

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35
Q

Where do specialised T cells in the gut sit?

A

Next to the epithelial cells: membrane:membrane proximity

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36
Q

Why do they sit so close?

A

So that they can target a specific cell and minimise the damage to the surrounding cells

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37
Q

Describe 4 proposed mechanisms of mucosal hyporesponsiveness

A

Anergy or deletion of antigen specific T Cells
Generation of regulatory T cells particularly CD4+ TGF Beta producing Th3 cells
Both immunosuppressive and induces switching of B cells to IgA production
Commensal organisms help regulate local hyporesponsiveness

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38
Q

How is a balance maintained between protective immunity and homeostasis?

A

Developed sophisticated means of discriminating between pathogen and innocuous antigens
Default response to oral administation of portein state of specific peripheral unresponsiveness - oral tolerance
T cell and IgE mediated reponses are inhibitored more than serum IgG responses both locally and systemically because these cause aggressive immune responses

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39
Q

In what state does mucosal dendritic cell maturation inhibited

A

In the presence of commensal bacteria,

40
Q

How do mucosal dendritic cells become active?

A

Invasive microorganisms penetrate epithelium

41
Q

Activated dendritic cells express what?

A

Strong co-stimulatory ligands

42
Q

What do immature dendritic cells give?

A

Weak co-stimulatory signals and induce CD4 T cells to differentiate into regulatory TH3 or Treg cells

43
Q

What do strong co-stimulatory ligands induce?

A

CD4 T cells to differentiate into effoector TH1 and TH2 cells

44
Q

Name the 3 distinct features of mucosal immune system

A

Anatomical,
effector mechanisms
Immunoregulatory environment

45
Q

Describe some of the anatomical features

A

Intimate relationship between mucosal epithelia and lymphoid tissue
Organised lymphoid structures unique to mucosal sites
Specialised antigen uptake mechanisms

46
Q

Describe some of the effector mechanisms

A

Activated / memory T cell predominate

Natural effector / regulatory T cells

47
Q

Describe some of the immunoregulatory environment

A

Active down regulation of immune response

Inhibitory macrophages and tolerising dendritic cells

48
Q

Why do rural children (living with high intestinal parasites loads) get less alllergy

A

They have exposure of the developing immune response to certain environmental microorganisms

49
Q

Describe the speed of innate mechanisms eliminating most intestinal infections

A

Rapid

50
Q

How does activation of mucosal immune responses occur?

A

Activation through ligation of pattern recognition receptors (PRR)

51
Q

Why does everyone make slightly different immune responses?

A

Because of variations in our genetics

52
Q

What determines the outcome of infection by intestinal pathogens?

A

A complex interplay between the microorganism and the host immune response

53
Q

Name a classic example of a disease in which the outcome varies greatly?

A

Leprosy

54
Q

Describe coeliac disease

A

Geneticlaly linked, autoimmune disorder, causes damage to the small intestine leading to malnurtition as you can no longer absorb

55
Q

What type of viruses are thought to be a trigger?

A

Enteric viruses

56
Q

What happens if you do not have HLADQ2/ HLADQ8

A

You are genetically susceptible and there must be a T cell component

57
Q

Describe the changes that occur to the small intestine in Coeliac’s disease

A

Flattened epithelial cells
Small intestine has scalloping
Small intestine with villous atrophy instead of normal finger like projections
Epithelial cells get more and more ragid
Packed full of cells (cellular infilitrate)
Hugely reduced surface area = hugely reduced absorption

58
Q

What does the MARSH score tell us?

A

The level of celiac disease (0,1,2,3a,3b,3c) 0 = normal 3c = total atrophy

59
Q

As damage recedes, the ragged, lymphocyte infiltrated enterocytes are replaced by what type of cells?

A

Normal columnar ones

This assures normal transport from the lumen into the body

60
Q

What happens if epithelial cells express a stress marker?

A

The intraepithelial lymphocyte cells will kill the epithelial cells

61
Q

What initiates the stress response in the cells causing lymphocytes

A

Gluten peptides

62
Q

What is the function of transglutaminase and where is it found?

A

To modify gluten peptides

found in all epithelial cells

63
Q

What does the modfied peptide bind to?

A

MHC class 2 molecules

64
Q

What does the bound peptide then go on to activate?

A

Gluten-specific CD4 T cells

65
Q

What do the gluten specific T cells then do?

A

Target epithelial cells which have fluten peptide in them as it think that the gluten is a virus

66
Q

What type of immune response is a gluten intolerance?

A

Innapropriate

67
Q

What do we do for everybody complaining of gluten intolerance

A

Antibody test (screening test to see hwo needs to further tests)

68
Q

What do we do for people who are positive for the anitbody test?

A

Biopsy them

69
Q

How do we diagnose children?

A

Through serology and genetics.

70
Q

What happens if a patient has not eaten gluten?

A

There will be a false negative. THe patient will then have to go back on to gluten for 6 weeks before being tested again

71
Q

What is the main cause of persistant symptoms?

A

Lack of compliance

72
Q

Who are more likely to have Caeliacs disease?

A

Patients who are IgA deficient

73
Q

The proper development and function of the intestinal immyne systemic is dependent on what?

A

Specific microbiota which have evolutinonary co-evolved

74
Q

What does Inflammatory bowel disease prevent?

A

The invasion of harmful pathogens while remaining tolerant to innocuous food substances and commensal micro-organisms

75
Q

What might lead to inflammatory bowel disease?

A

An altered function and imbalance of the relationship between the immyne system and tolerance to innocuous food substances

76
Q

Where is the site of Ulcerative Colitis?

A

Colon

77
Q

What inflammation occurs in Ulcerative Colitis?

A

Mucosal (superficial)

78
Q

What does smoking do in Ulcerative Colitis do?

A

Protects

79
Q

What cytokine profile is involved in xUlcerative Colitis?

A

Th2 IL-5/13

80
Q

What genetic factors are involved in Ulcerative Colitis?

A

HLADR2

81
Q

Where does Crohn’s disease occur?

A

Any part of the GI tract

82
Q

What inflammation occurs in Crohns disease

A

Transumral / granulomatous

83
Q

What cytokins are you present in CD profile?

A

Th1, IL23, gamma IFNG

84
Q

Granulommas are always associated with what type of responses?

A

Th1 responses

85
Q

Describe the inflammation in Crohn’s disease

A

Focal and discontinuous inflamation with deep and eroding fissures +/- granulomas

86
Q

What factors contribute to Crohn’s disease

A

Multiple genetic deficiency and immunologic mechanisms

87
Q

What is the gene which has been identified in Crohn’s disease?

A

NOD2

88
Q

Where does ulcerative colitis occur?

A

The rectum and colon

89
Q

What way does ulcerative colitis move?

A

Proximally and contiguously (touching eachother)

90
Q

What occurs in the surface mucosa?

A

Inflammation and ulceration

91
Q

Where do all of these diseases occur?

A

Urbanised westernised societies

92
Q

Both conditions produce large amounts of what?

A

Inflammatory cytokines

IL-1, IL-6 and TNF alpha

93
Q

How can we treat these types of disorders?

A

Non specific anti-inflammatory and immunosuppressive drugs, steroids, azathiprine, cyclosporin, methotrexate

94
Q

What type of reaction is a food allergy ?

A

Type 1 hypersensitivity reaction

95
Q

How is a reaction initiated?

A

By cross linking of allergen specific IgE on the surface of mast cells with the specific allergen

Gastro (67 decks)

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