Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal > Immunology > Flashcards

Immunology Flashcards

1
Q

Why are mucosal tissues highly vulnerable?

A

Due to their fragility and permeability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of lymphoid tissue is important in mucosal immunity?

A

Secondary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do dendritic cells enter a lymph node?

A

Through afferent lymphatic vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where do T cells enter a lymph node?

A

Through blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does it mean when it is said that the gut epithelium has an intimate relationship between mucosal epithelia and lymphoid tissue?

A

That they are very close and there are organised lymphoid structures unique to the mucosal site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the main type of T cells present?

A

Activated/memory T cells predominate, also natural effector/regulatory T cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What 2 types of cells make the mucosa an immunoregulatory environment?

A

Inhibitory macrophages and tolerising dendritic cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the equivalents of lymph nodes in the small and large intestine?

A

Small: Peyer’s patch.
Large: isolated lymphoid follicle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Other than these structures, where else are lymphocytes located in the mucosa?

A

Lamina propria and in the epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are M cells and what do they cover?

A

They are specialised cells with characteristic membrane ruffles that let antigens in. They are part of the epithelial layer that covers Peyer’s patches.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the 3 steps involving M cells and dendritic cells which cause activation of T cells.

A
  1. M cells take up antigen by endocytosis and phagocytosis.
  2. Antigen is transported across the M cells in vesicles and are released at the basal surface.
  3. Antigen is bound by dendritic cells, which activate T cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is it possible for dendritic cells to capture antigens from the lumen of the gut?

A

They can extend their processes across the epithelial layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 2 receptors on T cells that allow them to enter Peyer’s patches?

A

Homing receptors CCR7 and L-selectin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

After T cells have been activated by dendritic cells, where do they then go?

A

They drain via mesenteric lymph nodes to the thoracic duct and return to gut via the bloodstream.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do gut-homing effector T cells bind to on endothelium?

A

MAdCAM-1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are T cells moved from the endothelium to the epithelium of the gut?

A

Through the chemokines that gut epithelial cells express specific for gut-homing T cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What allows lymphocytes primed in the gut to migrate to other mucosal sites?

A

MAdCAM is also found in the vasculature of other mucosal sites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is an example of the common mucosal immune system involving mothers and children?

A

There is passive immunity transfer in breast milk as the T cells for the gut pathogen encountered will be present in the mucosa of the breast tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a downside to the common mucosal immune system?

A

It makes vaccine development difficult for some reason.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the predominant Ig in the gut?

A

IgA (then IgM then IgG).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the difference between IgA in the gut and in the systemic immune response?

A

IgA in gut is dimeric, in systemic immune response is monomeric.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does IgA bind to that allows it to be endocytosed through the epithelial cells into the lumen of the gut?

A

Poly-Ig receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens to the poly-Ig receptor as the IgA transfers to the gut lumen?

A

Enzymes cleave it to form a secretory components on the IgA which protects the connected bit of both IgA molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 3 ways that IgA helps mucosal immunity?

A
  1. Secreted IgA on the gut surface can bind and neutralise pathogens and toxins.
  2. IgA is able to bind and neutralise antigens internalised in endothelial cells.
  3. IgA can export toxins and pathogens from the lamina propria while being secreted.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why are most people who are IgA deficient asymptomatic?

A

Because IgM can replace IgA when it has to as it is also polymeric.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the majority of the intraepithelial lymphocytes?

A

T cells, mostly CD8+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Are intraepithelial T cells activated or inactivated?

A

They are activated containing full killing machinery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Expression of what integrin anchors intraepithelial lymphocytes in the epithelium?

A

AlphaE@beta7.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Do intraepithelial lymphocytes have a broad or restricted antigen receptor repertoire?

A

Restricted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How many types of intraepithelial T cells are there and how do they differ?

A

2, they have different recognition mechanisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the immunological pathway involving viral infection of a mucosal epithelial cell?

A

Infected cell displayes viral peptide to CD8 IEL via MHC class I. Activated IEL kills infected epithelial cells by perforin/granzyme and Fas-dependent pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the immunological pathway involving stress of an epithelial cell as a result of infection, damage or toxic peptides?

A

They express MIC-A and MIC-B. Activated IEL kills the stressed cell via the perforin/granzymes pathway.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What happens when the CD8+ T cells kill more epithelium than is produced?

A

You get a flattened epithelium will less villi e.g. coeliac disease. Causes malabsorption.

34
Q

How does our body maintain the balance between protective immunity and homeostasis?

A

It has developed sophisticated means of discriminating between pathogen and innocuous antigens.

35
Q

Responses mediated by what cell/Ig are inhibited more than others and why?

A

T cell and IgE more than IgG, they locally and systemically cause the most damage.

36
Q

What organisms help prevent hyperresponsiveness in the gut and how?

A

Commensal organisms through PPAR gamma.

37
Q

What type of T cells are immunosuppressive and what do they do?

A

Regulatory T cells particularly CD4+ TGF beta producing Th3 cells (weak costimulation). Induce switching of B cells to IgA production.

38
Q

What is the difference of the effect on dendritic cells that commensal bacteria and invasive microorganisms have?

A

Commensal bacteria inhibit dendritic cell maturation. Invasive microorganisms penetrate epithelium to activate dendritic cells.

39
Q

What do pathogens bind to which allows innate mechanisms to eliminate most intestinal infections rapidly?

A

Pattern recognition receptors.

40
Q

What are the 3 substances produced by the innate immune response in an intestinal infection?

A

Cytokines, chemokines and defensins.

41
Q

When a CD4+ T cell is activated in the intestine, what can it differentiate into and what will their effects be?

A

Th1 or Th2 helper cell. Th2 has a protective effect, Th1 causes host damage.

42
Q

What are the 4 functions of Th2 cells, going from most protective to most damaging?

A
  1. Produce IL-13 which induced epithelial cell repair and mucus.
  2. Produces IL-5 which recruits and activates eosinophils.
  3. Drive B cells to produce IgE.
  4. Drive mast cell recruitement via IL-3, IL-9. Specific IgE arms mast cell against helminths.
43
Q

What are the 2 functions of Th1 cells, going from most to least damaging?

A
  1. Activate B cells to produce IgG2a.

2. Th1 cells activate macrophages.

44
Q

What immune cell produces a response that cannot clear a parasite?

A

Th1.

45
Q

Why is HIV so devastating to T cells?

A

The mucosae has most of the memory T cells.

46
Q

What do symptomatic people get with an IgA deficiency?

A

Recurrent bacterial sinopulmonary infections.

47
Q

What is common variable immune deficiency (CVID)?

A

Failure of stem cells to differentiate into Ig secreting cells.

48
Q

What can CVID cause?

A

Recurrent bacterial sinopulmonary and GI infections.

49
Q

What is XLA?

A

x-linked agammaglobulinaemia.

50
Q

When does XLA present?

A

7 and 8 months of age.

51
Q

What is there none of in XLA?

A

B cells or Ig.

52
Q

What are the signs of XLA?

A

Sinopulmonary and GI infections and devastating manifestations of chronic enteroviral infections.

53
Q

What is the underlying cause of chronic granulomatous disease?

A

Failure of phagocyte burst, neutrophils can’t kill things.

54
Q

What can chronic granulomatous disease present with?

A

Pneumonia, liver abscess, perianal abscess and skin abscess.

55
Q

What is the only treatment of chronic granulomatous disease?

A

Bone marrow transplant.

56
Q

What is SCID?

A

Severe combined immunodeficiency.

57
Q

What is the underlying cause of SCID?

A

Defect in T and B cell immunity.

58
Q

What can SCID cause?

A

Oral candidiasis, chronic diarrhoea, interstitial pneumonitis, CMV/rotavirus/EBV.

59
Q

What type of organisms are infections in SCID?

A

Fungi and viruses.

60
Q

Why are venoms and drugs more likely to cause anaphylaxis?

A

They are given systemically.

61
Q

Is coeliac disease an allergy?

A

No as it is not IgE mediated, it is T cell mediated.

62
Q

What mutations give you a genetic susceptibility to coeliac disease?

A

HLADQ2/HLADQ8.

63
Q

At what age can coeliac disease present?

A

Any age.

64
Q

What causes the activation of IEL in coeliac disease?

A

Gamma interferon from gluten specific T cell activates epithelial cells which produce IL-15 which induces proliferation and activation of IEL.

65
Q

What is the enzyme that gliadin peptide (from gluten) is in complex with when it crosses the epithelium?

A

Tissue transglutaminase (TTG).

66
Q

What is the gold standard investigation for coeliac disease (not required in paediatrics)?

A

Biopsy.

67
Q

What is looked for in serology when screening for coeliac disease?

A

IgA anti-tissue transglutaminase autoantibodies.

68
Q

What primary immunodeficiency will cause a false negative for serology in coeliac disease and how would these people have to be diagnosed?

A

IgA deficiency, biopsy.

69
Q

How long will patients need to have eaten gluten for to make the serology work?

A

6 weeks.

70
Q

What else is serology used to monitor if someone is known to have coeliac disease?

A

Dietary compliance monitoring.

71
Q

What has to happen to a B cell for it to make anti-tTG cantibodies?

A

It has to bind to a CD4+ T cell which then activates the B cell.

72
Q

Where can Crohn’s disease affect and where does it affect most often?

A

Any part of the GI tract. Most often distal ileum and colon.

73
Q

Describe what would be seen in a pathological specimen of Crohn’s disease?

A

Focal and discontinuous inflammation with deep and eroding fissures with granulomas.

74
Q

What type of T cells is Crohn’s disease mediated by and what cytokines do they produce?

A

Th1, gamma interferon, IL-12, TNF alpha.

75
Q

Give an example of a gene that was identified to cause Crohn’s disease and what does it code for?

A

NOD2 - intracellular pattern recognition receptor (PRR).

76
Q

Where does ulcerative colitis usually begin and where does it move to?

A

Starts in rectum and moves proximally and contiguously.

77
Q

Give some examples of extra-intestinal manifestations that ulcerative colitis can develop.

A

Arthritis/uveitis, skin lesions.

78
Q

What would you see in a histological specimen of ulcerative colitis?

A

Distortion of the crypts with infiltration of monocytes/neutrophils and plasma cells.

79
Q

Where is inflammation and ucleration restricted to in ulcerative colitis?

A

Surface mucosa.

80
Q

Does ulcerative colitis fit into the Th1/Th2 split?

A

No.

81
Q

What is the suspected immunopathology of ulcerative colitis?

A

NK T cell mediated disease via IL-13.

Gastrointestinal (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions