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Immunology Flashcards

1
Q

What are the physiological functions of mucosal tissues?

A

Gas exchange
Food absorption (vitamin absorption and production)
Sensory activities
Reproduction

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2
Q

As well as portals of entery for pathogens, mucosal surfaces are also portals of entry for non pathogenis antigens. T of F?

A

True. Things like food.

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3
Q

What type of epithilium lines the small intestine?

A

Single columnar epithilium

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4
Q

Define transcellular and paracellular

A 
Transcellular = transport through a cell eg glucose from the lumen to the blood
Paracellular = transport between cells- in the interstitail fluid
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5
Q

What are the mucosal organs of the human?

A

Salivary gland, mamory gland, kindeys, Uterus, bladder and vagina

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6
Q

What are the mucosal surfaces of the body?

A

Conjunctiva, oral cavity, Trachea, sinus, lungs, oesophagus, stomach, lange and small intestines uterus, bladder and vagina

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7
Q

An immune response at one mucosal site can initiate an immune response at all mucasal sites?

A

Yes

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8
Q

What are the secondary lymphiod tissues?

A

Lymph nodes and spleen

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9
Q

What are the primary lymphiod tissues?

A

Bone marrow and thymus

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10
Q

Where are lymph nodes located?

A

All mucosal surfaces

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11
Q

How do dendritic cells enter lymph nodes?

A

Afferent lymph vessels

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12
Q

How do T and B lymphocytes enter lymph vessels?

A

In the blood

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13
Q

Where do antigen presenting cells go when they first enter the lymph node?

A

Paracortical area and look for a T cell with a TCR complementary to the MHC class 2 protein and peptide antigen

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14
Q

Where are classical lymph nodes found?

A

In the messentary- not the gut wall

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15
Q

What is an intra epithilial lymphocyte?

A

CD8+ T lymphocytes

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16
Q

Where are the antigens detected in the small intestine?

A

Peyers patch

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17
Q

Where are the antigens detected in the large intestine?

A

Isolated lymphoid follicle

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18
Q

Where iare the immune effector functions taking place in the gut?

A

Lamina propria

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19
Q

What effector cells can be found in the lamina propria?

A

All the immune cells from the blood

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20
Q

How do antigen presenting dendritic cells get to lymph nodes in the mesentary?

A

Afferent lymph vessels

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21
Q

What epithilium covers the peyer’s patch?

A

Dome epithilium

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22
Q

What are M cells and where are they found?

A

M cells are ‘microvilli’ cells as they increase the surface area for sampling antigens. Found just above the peyer’s patch interspersed in the epithilial cells

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23
Q

Where are dendritic cells found in the Peyer’s patch?

A

Directly under M cells with dendritic processes within the M cells

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24
Q

When a dendritic cell presents an antigen with in the peyer’s patch, what happens next?

A

Activates T cells partially which then travel to lymph nodes in the messentry to be fully activateand then directed back to the lamina propria of the intestine.

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25
Q

Are germinal centres present in peyer’s patches?

A

Yes

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26
Q

How do M cells take up antigens from the lumen and how do they become bound to dendritic cells?

A

Endocytosis or phagocytosis. It is transported across the M cell in vesicles and released at the basal surface where the antigen is bound to dendritic cells

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27
Q

Can dendritic cells extend processes across the epithilial layer to directly capture antigens from the lumen of the gut withiut an M cell?

A

Yes. This happens in the lungs and GI tract

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28
Q

What are the immune cells of the epithilial layer in the gut?

A

Dendritic cells

CD8+ T lymphocytes are intraepithilial lymphocytes

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29
Q

What are the immune cells of the lamina propria?

A

Dendritic cells, Macrophages, CD4+ T cells, Mast cells, Plasma cells, IgA

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30
Q

What are plasma cells?

A

Termiinally differentiated B cells which produce antibodies

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31
Q

What directs unactivated T cells into the Peyer’s patch from blood vessels?

A

Homing receptors CCR7 and L-selectin

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32
Q

How do activated T cells in the mesenteric lymph nodes get back to the gut where the infection is?

A

Drain into the thoracic duct and enter the blood stream via the left venous angle.
The activated T cells express alpha4 beta 7 integrin and CCR9 which hone on the lamina propria

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33
Q

What molecules does the endothilium in the get express which enables activated T cells to bind and transendothilially migrate into the lamina propria?

A

MAdCAM-1

MA = Molecular adressin

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34
Q

Activated T cells in the lamina propria migrate to the gut epithilial cells due to what?

A

Chemokines expressed by the epithilial cells which the activated T cells have receptors for

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35
Q

MAdCAM is also found in the vasculature of other mucosal sites. What are the implications for this?

A

An immune response in the gut will also produce an immune response at other mucosal sites because the lymphocytes primed in the gut can migrate

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36
Q

There is a unified reirculation compartment meaning there is a common mucosal immune system. T or F?

A

True

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37
Q

What is the beifit of the common mucosal immune system for babies?

A

The antibodies and being produced in response to the pathogens in the mothers gut can be transferred to the baby for passive immunity through breast milk

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38
Q

What challenges does the mucosal immune system present?

A

Vaccine development. Hard to create a vaccine that is given systemically that will elicit a mucosal response. Eg HIV for which the primary infection site is the urogenital tract.

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39
Q

Which antibodies are produced by the mucosal response in the gut?

A

80% IgA
15% IgM
5% IgG

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40
Q

What is special about mucosal IgA?

A

IgA1:IgA2 ratio is 3:2 (its 10:1 in peripheries)
IgA2 is less prone to cleavage by enzymes than IgA1
IgA is a dimer in mucosal tissue and a monomer
in periferies

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41
Q

What is the J chain?

A

Joining chain connecting 2 IgA monomers to produce a dimer

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42
Q

How is IgA secreted into the lumen?

A

IgA dimer released from plasma cells in the lamina propria binds to the poly Ig receptor on the basolateral surface of epithilial cells.
The antibody receptor complex is endocytosed and travels to the apical membrane where it is released with the a secretory component

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43
Q

What is the function of the secretory component of IgA?

A

It wraps around the hinge region which is most prone to enzymatic cleavage. Protects the IgA.

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44
Q

What is the functions of sIgA in the gut?

A

1) Bind and neutralise pathogens and toxins in the lumen
2) Bind and neutralise antigensin internalised endosomes
3) Export toxins from the lamina propria while being excreted

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45
Q

The IgA secreted by plasma cells is specific to what?

A

The antigens that were detected in the peyer’s patch

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46
Q

1 in 300 people are IgA deficient in Tayside. Why are they asymptomatic?

A

IgM can replace IgA because the poly Ig receptor on the basolateral membrane of epithilial cells can also bind IgM because it is a polyer too (pentemer)

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47
Q

Intraepithilial lymphocytes are mostly CD8+ T cells. What are the featres of these cells?

A

Fully activated for killing (no cytokines required)

Restricted antigen receptors so are very specific

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48
Q

What immune cell is responsible for coelliac disease?

A

Intraepithilial lymphocytes

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49
Q

What anchors intraepithilial cells into the membrane (every 10 cells) to prevent them moving?

A

AlphaEpsalon:Beta7 integrins

50
Q

What types of cells will intraepithilial cells kill?

A

Virally infected mucosal cells with MHC class 1
Epithilial cells under stress due to infection, damage or toxins which express MIC-A and MIC-B
which binds to NKG2D on IEL

51
Q

How do intraepithilial cells kill detected cells?

A

Perforin/granzymes
Fas dependent pathways
Only kill specific cells- not surrounding cells

52
Q

What happens if intraepithilial cells are killing more cells than epithilail stem cells are producing?

A

Flattened epithilium and reduced absorption. CLinically present with mal absorption

53
Q

How does coelliac disease present?

A

Malabsorption

54
Q

What is oral tollerence?

A

Oral tolerance is classically defined as the suppression of immune responses to antigens (Ag) that have been administered previously by the oral route. Multiple mechanisms of tolerance are induced by oral Ag. Low doses favor active suppression, whereas higher doses favor clonal anergy/deletion.

55
Q

Why are T cell and IgE mediated responses inhibited more than serum IgG in oral tolerance?

A

Because T cells and IgE cause the most damage

56
Q

What are the mechanisms of mucosal HYPOresponsiveness for food?

A

1) Commensal organisms of the gut
2) Anergy or deletion of antigen specific T cells => no costimulation
3) Generation of T reg cells which => T helper 3 cell production. Suppresses the immune system and switching B cells to IgA production

57
Q

Toll Like receptors recognise a ‘pathogen’ (food) which activates IKK. IKK phosphoryates IkB so its degraded and NFkB can translocate to the nuclus for gene transcription. How can this be prevented?

A

Commensal bacteria can activate PPARgamma which removes NFkB from the nucleus
OR commensal bacteria can block degradation of phosphorylated IkB so NFkB cannot translocate to the nucleus

58
Q

What do commensal bacteria produce that inhibits dendritic cell maturation?

A

TGF beta and TSLP

59
Q

What response do immature and mature dendritic cells initiate?

A

Immature => weak co-stimulation => T reg cells and T helper 3 cells

Mature => strong co-stimulation =>T helper 1 and T helper 2 cells

60
Q

Can you summarise the mucosal response to infection with a pathogen to the point of activating immune cells?

A

1) Bacteria are endocytosed and recognosed by toll like receptors in vesicles or bacteria directly enter the cytosol of the epithilial cells and recognised by NOD1/2.
2) These activate the NFkB pathway => gene transcription and production of cytokines, chemokines and defensins.
3) These activate macrophages neutrophils and dendritic cells.

61
Q

The outcome of an infection by a pathogen can have a protective or a damaging effect on the host. What determine what type of effect is produced?

A

Immunogenetics. Some people have a very protective effect, for some there is more damage but there is a sliding scale.

62
Q

Helminth infection: nieve CD4+ T cells are activated and what will produce a protective response?

A

T helper 2 cells.

1) Produce IL13
2) Produce IL5
3) Stimulate B cells to produce IgE
4) Produce IL3 and IL9 which drive mast cell recruitment (important in helminth infections)

63
Q

Helminth infection: What does the production of IL13 lead to?

A

Epithilial cell repair and mucus.
Increased cell turnover aids sheeding of infected
cells and mucus helps sweep things out of the GI tract

64
Q

Helminth infection: What does IL5 lead to?

A

Recruitment and activation of eosinophils which produce MBP which kills paracites and mediates ADCC. It also promotes IgA production

65
Q

Helminth infection: What does production of IL3 and IL 9 lead to

A

Mast cells to produce mediatiors like histamine, TNF alpha that recruit inflammatory cells and remodel the mucus

66
Q

Helminth infection: nieve CD4+ T cells are activated and what will produce a damaging response?

A

Production of T helper 1 cells

1) Activate macrophages
2) Activate B cells to produce IgG

67
Q

Helminth infection, what is the consequence of Th1 cells activating macrophages?

A

Production causes tissue damage and tissue remodelling and release of pro inflammatory cytokines

68
Q

Helminth infection, what is the consequence of Th1 cells activating B cells to produce IgG?

A

I gG is a complement fixing antibody which is useless in helminth infections. Need antibodies bound to mast cells eg IgE

69
Q

What happens when the mucosal surface is exposed to HIV?

A

1) HIV invades dendritic cells which become activated and then migrate to the lymph nodes in the mesentery.
2) Nieve CD4+ T cells in the lymph nodes become infected and activated.
3) Activated T cells then move migrate back to the mucosal surface due to molecular adressins and HIV invades all the CD4+ T cells in the mucosal membranes.

HIV will kill 50-75% of memory T cells in the mucosal membrane. => Secondary immunodefficiency

70
Q

2/3 of people with selective IgA deficiency are assymptomatic. What type of infections are common in symptomatic individuals?

A

Sinopulmonary BACTERIAL infections.

Also coelliac disease is 10x more common in those with IgA deficiency

71
Q

What is CVID?

A

Common varient immunodefficiency is a primary immunodeficiency.

72
Q

When does CVID present?

A

Adulthood

73
Q

What are the common infections in those with CVID?

A

Recurrent sinopulmonary and GI infections. BACTERIAL

74
Q

What is the cause of CVID?

A

Failure to differentiate B cells in to Ig secreting plasma cells => Low IgG, IgA, IgM and IgE. This effects the adaptive immune response

75
Q

CVID has a diagnostic delay of 5-7 years. WHat is the consequence of this?

A

When CVID is picked up late they have bronchiectasis

76
Q

How is CVID treated?

A

Immunoglobulins

77
Q

What is XLA?

A

X linked agamaglobulemia. Affecting boys. Do not produce B cells or IgG

78
Q

When does XLA present?

A

7-8 months when maternal IgG is weaning

79
Q

What are the common infections in someone with XLA?

A

Sinopulmonary and GI infections. Bacterial.

and devastating manifestations of enteroviral infections.

80
Q

How is XLA treated?

A

Replacement immunoglobulins

81
Q

What is CGD?

A

Chronic granulomatous disease is caused by failure of the phagocyte respiratory burst

82
Q

What is the phagocyte respiratory burst?

A

NADPH oxidase => superoxide => reactive free radicals => kill pathogens

83
Q

WHat are the common infections in those with CGD?

A

Staph aureus, inflammatory granulomas, pneumonia, liver abscess, perianal abscess and skin abcess

84
Q

How many genes can cause CGD?

A

4

1 is X linked and 3 are autosomal recessive

85
Q

How is CGD treated?

A

Bone marrow transplant

86
Q

What is SCID?

A

Severe combined immunodefficiency. T cell gene defect which leads to a B cell defect.

87
Q

When does SCID present?

A

First weeks of life

88
Q

What are the common infections with SCID?

A

Oral candiditis, chronic diarrhoea, intestinal pneumonitis, rota virus, EBV

89
Q

Can haloallegens produce anaphylaxis?

A

No (thats things like pollen, dust mites etc)

90
Q

What is a food allergy?

A

Type 1 hypersensitivity reaction initiated by cross linking of allergen specific IgE bound to mast cells by Fc receptors with the specific allergen. Memory response- immune system must be primed.

91
Q

What are the classic triggers for anaphylaxis?

A

Venom and drugs because they are given systemically

92
Q

What is the common presentation of food allergy?

A

D&V, anaphylaxis is uncommon

93
Q

Whay can food cause anaphylaxis?

A

Absorption of whole food proteins across the gut- specific proteins which are very stable and not broken down by heat or gut enzymes

94
Q

What type of immune respose is an allergy?

A

Adaptive, IgE mediated

95
Q

Why is avoidance the best advice for someone with a food allergy?

A

The more times you present and antigen to the immune system the better (worse for the patient) the response is

96
Q

What is coeliac disease??

A

Gluten sensitive enteropathy

97
Q

Is coeliac disease an allergy?

A

No- its T cell mediated and is a hypersensitivity reaction

98
Q

What is the genetic susceptibility for coeliac disease?

A

HLADQ2- 95% of those with coeliac have this gene

HLADQ8- 5% of people with coelliac disease have this gene.

99
Q

Why is genetic testing not really useful for coeliac disease?

A

Because 20% of the general population haev HLADQ2 and they do not have coeliac disease

100
Q

What are the main immune cells involved in coeliac disease?

A

T cells and intraepithilial lymphocytes

101
Q

Once a gluten specific T cell is activated what happens?

A

interferon gamma from the T cell activates epithila cells which produce IL15 which induces proliferation and activation of intraepithilial lymphocytes. Both T cells and IEL can kill epithilial cells under stress

102
Q

When does coeliac present

A

Any age

Most often 20-40

103
Q

What are the macro and histopatholocial findings in coeliac disease?

A

Scalloping, Flattened epithilium/villous atophy, Only crypts remain.

104
Q

Which sub molocule of gluten produces coeliac disease?

A

Gliadin

Gluten is found in rye, wheat and barley

105
Q

Why are IgA antibodies for anti-gliadin and anti tissue transglutaminase produced in coelic disease?

A

Because when Gliadin passes through the epithilium it combines with the tissue transglutaminase enzyme and forms a complex which an antibody is produced for

106
Q

Activation of a CD4+ T cell in coeliac disease leads to activation of which other immune cells?

A

T helper 1 cells, CD8+ T cells and NK cells which all produce cytokines which damage enterocytes

107
Q

How is coeliac disease diagnosed in an adult?

A

Serology using IgA antitissue transglutaminase auto antibodies is used to triage cases for biopsy.
A biopsy is the gold standard test

108
Q

How is coeliac disease diagnosed in children?

A

Non biopsy diagnosis. Biopsy would require GA in a child Serology test using IgA antitissue transglutaminase auto antibodies.

109
Q

The IgA antitissue transglutaminase auto antibodies test is 95% sensitive and 97% specific but what is the patient group for which this test is uninformative? What must be done to diagnose coeliac disease?

A

Thise with IgA deficiency. You get false negatives because they cannot produce IgA in the first place. They are also 10x more likely to have coelic so you must do a biopsy

110
Q

Patient: I have been having trouble with my diet ect but I have cut gluten out and no I fell better, can you just do the test for coelliac disease please?

A

No because you must have been eating gluten for 6 weeks before the test.
No gluten = no anti-tissue transglutaminase antibody

111
Q

Apart from diagnosis of coelliac what is the other use of IgA antitissue transglutaminase (IgA anti TTG) auto antibodies test?

A

Dietary compliance monitoring. No gluten in diet = No autoantibody

112
Q

What are the causes of persistent symptoms in coeliac disease?

A

Lack of dietary compliance Rarely T cell lymphoma

113
Q

What is the best antigen presenting cell in a primary and secondary immune response?

A 
Primary = dendritic cell
Secondary = B cell
114
Q

Why is an AUTO antibody formed in coelic disease?

A

The gluten-
TTG complex binds to the B cell antigen on the TTG part, not the gluten part => anti TTG antibodies produced which attack self cells

115
Q

What part of the GI tract does Chron’s disease affect?

A

Any pary from mouth to annus. Most common in the terminal illeum and colon

116
Q

What are the characteristic tissue chages of Crohn’s disease?

A

Focal and discontinuous inflammation with granulomas. Very inflammatory T cell response

117
Q

There are over 200 genes associated with crohn’s disease. WHat is the nmost common?

A

NOD2 deficiency

118
Q

Where does ulcerative colitis effect the gut?

A

Begins in the rectum and moves proximally and continuously to the colon

119
Q

Which of UC and Crohns have extra intestinal symptoms?

A

Both

120
Q

What are the characteristic tissue changes in UC?

A

Distortion of the crypts with infiltration of monocytes, neutrophils and plasma cells. Inflammation only in surface mucosa

121
Q

What is the treatment for Crohns and UC?

A

Steroids and immunosupressive drugs

Anti TNF alpha

GI (48 decks)

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