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Eukaryotic Microbio > Immunology > Flashcards

Immunology Flashcards

1
Q

When was small pox officially eradicated?

A

1979

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2
Q

Why are all diseases not eliminated?

A
  • Antibody vaccines work well and are easy to design
  • Not all pathogens are controlled by antibodies
  • Not all pathogens maintain the same antibody targets over time
  • Kinetics, location and interplay between pathogen and host
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3
Q

Where is the largest portion of the immune system?

A

In the mucosal tissues of the human body. Nearly 3/4 of all lymphocytes are associated with the mucosa. Also the immunoglobin is associated with mucosa.

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4
Q

How is immune response initiated?

A

Innate cells respond to changes in tissues and invading objects

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5
Q

What counts as intracellular type 1 immunity?

A
  • Macrophage (bacterial/viral infections)
  • Dendritic cell (chronic inflammation)
  • Neutrophil (chronic inflammation)
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6
Q

What counts as extracellular type 2 immunity?

A
  • Eosinophil (worm/viral infections)
  • Basophil (allergic inflammation)
  • Mast cell (allergic inflammation)
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7
Q

What do macrophages do?

A

Macrophages act to phagocytose foreign objects but also reduce inflammation and increase wound healing

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8
Q

What do dendritic cells do?

A

Dendritic cells collect molecules from tissue and – if stimulated by specific signals will migrate to lymph node and initiate immune responses

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9
Q

What do neutrophils do?

A

Neutrophils are little packets of defensive molecules ready to respond quickly and kill invading pathogens. Can cause tissue damage too

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10
Q

What do eosinohils do?

A

Varieties of innate cells target different types of pathogen

Killing of antibody coated parasites

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11
Q

What do basophils do?

A

Varieties of innate cells target different types of pathogen

Promotion of allergic responses and augmentation of anti-parasitic immunity

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12
Q

What do mast cells do?

A

Release of granules containing histamine and active agents

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13
Q

What are peyers patches?

A

Peyers patches are covered by an epithelial layer containing specialised cells called M cells which have characteristic membrane ruffles

They go out and provide an antigen

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14
Q

What are mucosal tissues?

A

They are entry site for pathogens

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15
Q

What is the highest amount of worldwide deaths from mucosal diseases?

A 
Acute respiratory infections 4 million
Diarrheal diseases - 2.2m
HIV/AIDS - 2 m
Tuberculosis - 1.5m
Measles - 400,000
Whooping cough - 294,000
Hepatitis B - 103,000
Roundworm and hookworm - 6000
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16
Q

What are the friendly micobes that harbour mucosal tissues?

A 
Firmicutes
Bacteriodetes
Actinobacteria
Proteobacteria
Other Phyla
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17
Q

What are the distinctive features of the mucosal immune system?

A

Anatomical features - Imtimate interactions between mucosal epithelium and lymphoid tissues

Effector mechanisms - Multiple activated ‘natural’ effector/regulatory T cells present

Presence of distinctive microbiota

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18
Q

Where are intestinal lymphocytes found?

A

In organised tissues where immune responses are induced and scattered throughout the intestine, where they carry out effector functions

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19
Q

What are resident memory cells?

A

Big target of vaccine design

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20
Q

What is the waldeyer’s ring?

A

The tonsils and adenoids form a ring of lymphoid tissues around the entrance of the gut and airway

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21
Q

What do M cells do?

A

They take up antigen by endocytosis and phagocytosis

Antigen is transported across the M cells in vesicles and released at the basal surface

Antigen is bound by dendritic cells which activate T cells

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22
Q

How does the mucosa exist?

A

As one large immune tissue

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23
Q

What does the mucosal immune system consist of?

A
  • The epithelium

- Lamina properia

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24
Q

What does the lamina properia contain?

A
  • CCR9 cells
  • macrophages
  • mast cells
  • dentritic cells
  • IgA
  • CD8 T cell
  • Plasma cell
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25
Q

What does the epithelilal layer contain?

A
  • Homing receptors

- Macrophages in wall

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26
Q

What are homing receptors?

A

Cells binds in to a bunch of receptors

Allows T cells to come in to the mucosal area

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27
Q

What does the mucosa do in the gut?

A

It drives T cell responses which home back to the mucosa

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28
Q

What happens when we get a T cell response in the mucosa?

A

The interaction T cells receive, it tells the cell to up regulate markers

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29
Q

What do intergrins do?

A

Bind and function cells in an area

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30
Q

What is on all the T cells that have been activated at the gut?

A
  • a4B7 molecule
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31
Q

What do gut homing effectors do?

A

They bind MAdCAM 1 on endothelium through recognition from a4B7 molecule

Gut epithelial cells express chemokines specific for gut-homing cells

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32
Q

What is E-cadherin bound by?

A
  • aEB7 molecule
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33
Q

What are the 4 varieties of pathways of which the mucosal barrier can allow antigen to pass?

A
  • Nonspecific transport across epithelium
  • FcRn dependent transport
  • Apoptosis- dependent transfer
  • Antigen capture

Each of these mechanisms gives a different result

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34
Q

What is Nonspecific transport across epithelium?

A

The enterocytes bring across antigens

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35
Q

What is FcRn- dependent transport?

A

Immunoglobin gets bound to pathogen and take it to the dendritic cell

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36
Q

What is apoptosis-dependent transfer?

A

Epithelial cells die in situ and allows for the carrying of vesicles which can then be delivered to the dentrictic cell

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37
Q

What is antigen capture?

A

The antigen gets reached through the mucosal barrier by dendritic cells

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38
Q

What are effector cells within the mucosa?

A

Lymphocytes called intraepithelial lympocytes (IELs) lie within the epithelial lining of the gut

They are largely CD8-postitve T cells

The IELs can be seen to lie within the epithelial between epithelial cells

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39
Q

How do effector cells respond to pathogens?

A
  1. Virus infects mucosal epithelium cell
  2. Infected cell displas viral peptide to CD8 IEL via MHC class I
  3. Activated IEL kills infected epithelial cell by perforin/granszyme and Fas-depended pathways
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40
Q

Why is it good to kill the epithelial cell?

A

To kill the cell that contains the virus

Like killing the trojan horse

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41
Q

What is the immune mediated response due to stress or damage?

A
  1. Epithelial cells undergo stress as a result of infection, damage, or toxic peptides, and express MIC-A and MIC -B
  2. NKG2D on IEL binds to MIC-A, B and activates the IEL. CD8a:a homodimers also bind to TL
  3. Activated IEL kills the stressed cell via the perfonin/granzyme pathway
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42
Q

What is IgA antibody?

A

A unique antibody secreted into the mucosal lumen

It protects the mucosa

Binds up toxins and neutralise pathogens

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43
Q

What is the IgA antibodies pathway?

A
  1. Binding of IgA to receptor on basolateral face of epithelial cell
  2. Endocytosis
  3. Transcytosis to apical face of epithelial cell
  4. Release of IgA dimer at apical face of epithelial cell
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44
Q

What results of a transcriptional profile which then results in inflammation in the mucosa?

A

The same principals of pathogen associated molecular pattern recognition by pattern recognition receptors

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45
Q

How does salmonella affect the gut microbiota?

A
  1. Salmonellae enter and kill M cells, and then infect macrophages and epithelial cells
  2. Salmonellae invade the luminal surface of epithelial cells
  3. Salonellae enter phagocytic cells that are sampling the gut luminal contents
46
Q

What happens if defences fail in salmonella poisoning?

A

Salmonellae can enter the bloodstream and cause a system infection

47
Q

How does Shigella affect the gut?

A
  1. Shigallae penetrate gut epithelium through M cells
  2. Shigallae invade basal surface of epithelial cells and spread to other epithelial cells
  3. Shigella cell-wall peptides bind and oligomerise NOD1, activating the NFxB pathway
  4. Activated epithelum secretes CXCL8, recruiting neutrophils
48
Q

How does Clostridium difficle affect the gut?

A
  1. The colon is colonised by large number of commensal bacteria of which antibiotics kill
  2. Closterium difficle gains a foothold and produces toxins that cause mucosal injury
  3. Neutrophils and RBCs leak into gut between injured epithelial cells
  4. Connective tissue degretation leads to colitis and pseudomembrane function
49
Q

What are the new treatments for clostridium difficile?

A

Vancomycin and metronidazole

50
Q

What consists of activated TH1 cells?

A
  • IFN-y and CD40 ligand
  • Fas ligand
  • IL-2
  • IL-3 + GM-CSF
  • TNF-a + LT-a
  • CXCL2
51
Q

What are the 3 type of immunity against parasites?

A
  1. Antidisease immunity
  2. Antiparasite immunity
  3. Premunition
52
Q

What is antidisease immunity?

A

antidisease immunity, conferring protection against clinical disease, which affects the risk and extent of morbidity associated with a given parasite density

53
Q

What is antiparasite immunity?

A

antiparasite immunity, conferring protection against parasitemia, which affects the density of parasites

54
Q

What is premunition immunity?

A

premunition, providing protection against new infections by maintaining a low-grade and generally asymptomatic parasitemia

55
Q

What is the Th1/Th17 dependent pathology?

A
  • Hepatotoxicity (AST/ALT elevated)
  • Endotoxemia (Elevated serum LPS)
  • Little or no liver fibrosis
  • Classically activated macrophages
56
Q

What is Th2-dependent pathology?

A
  • Extensive liver fibrosis
  • Portal hypertension
  • Bleeding collateral vessels (gut)
  • Alternatively activated macrophages
57
Q

What is macrophage polarisation?

A

Macrophage polarization refers to how macrophages have been activated at a given point in space and time

Parasites manipulate macrophage polarisation

58
Q

What are the immune evasion mechanisms present to trypanosomatids?

A
  • Passive immune evasion by antigenic variation of the variable surface glycoprotein surface coat
    • Ab binding reduces parasite number in blood
  • Impact post receptor signalling in immune cells thereby reducing immune cell function
59
Q

How do parasites promote survival?

A

By manipulating the PRR pathways

60
Q

How to parasites reduce inflammation?

A

By down-regulating activation pathways

61
Q

Which regulatory cells are induced by parasites?

A
  • IL-2
  • TGF-B
  • Reg DC/IL-10
  • IL-12/IL-27
62
Q

How does the sand fly vector infect humans?

A

Goes into the skin and chops up the skin and creates a pool feeder

Causes inflammation

Parasites come in at the same time as the flies making a blood pool

The sand flies first bite blocks up the pathway, it cant get a probe meal

Parasitic infection makes the sand fly bite 3 times as it cannot bypass the blood feed

The neutrophils take up the leishmania

T cells receives signals not allowing it to be fully activated

When the sand fly bites, there’s no antibodies nearby

63
Q

What does the biting action of vector do?

A

Influences early skin responses and facilitates infection

64
Q

What does the male, female pairing in schistosoma need to do?

A

The make eggs

Wont occur unless received signals from host-derived factors

65
Q

Where do worms that infect have to sit in the body TO infect?

A

In the veins

Veins will clot and try to stop that vessel from working

Parasite produces molecules to induce blood clots, induce blood cell lysis and regulate a vascular tone

66
Q

What is the outcome of schistosoma eggs in men?

A

Liver cancer

Occurs more frequently in tropical areas

Also causes fibrosis and cirrhosis from excess collagen

67
Q

Why doesn’t this affect women?

A

The oestrogen regulates an action that drives fibrosis

68
Q

What are homoeostatic activities in parasites?

A

They result in chronic persistence and tissue damage

69
Q

How can parasites influence allergic responses?

A

They can perturb immune responses to other antigens and influence allergic and protective responses

E.g. people eating tapeworms to drive a regulatory environment, allergies might go away and to regulate immune response

70
Q

What is the immune response to pre-erythrocytic stage in malaria?

A
  • Antibodies are eventually developed against the most abundant surface protein on the sporozoite, which trap sporozoites in the skin and reduce their invasion into liver cells by inhibiting their motility
  • Liver cells can be destroyed by Ab-dependent cellular cytotoxicity or by the action of interferon-y-producing CD4+ and CD8+ T cells, NK cells and yg T cells
71
Q

What is the immune response to the blood stages?

A
  • A pro-inflammatory cytokine response involving IL-1B, 1L-6, IFNy, TNFa and IL-12 which enhances phagocytosis and killing of iRBCs by macrophages
  • However, over-production of these cytokines contributes to malarial pathology and down regulation of inflammation (by IL-10 and TGF-b) once parasitaemia is under control, is required to prevent severe disease.
  • Phagocytosis of iRBC is augmented by their opsonisation by cytophilic Abs binding to parasite antigens exported to the RBC surface.
  • However, these antigens are highly polymorphic and undergo clonal antigenic variation, meaning that effective opsonisation (or prevention of iRBC sequestration in blood vessels) may only develop after many and varied malaria infections.
  • Antigens expressed on merozoites are also polymorphic but Abs against conserved or semi-conserved epitopes can inhibit merozoite invasion of RBC.
  • Complement- fixing Abs against gametocyte and gamete antigens can prevent the establishment of infection in the mosquito and thereby block malaria transmission.
72
Q

What is adaptive immunity?

A
  • Slow response
  • Recognition is low affinity receptors
  • Response - T and B cells with receptors encoded by fully rearranged genes
  • Memory
73
Q

What is innate response?

A
  • Rapid response
  • Pattern recognition receptors-germ-line encoded
  • Increase of cytokines for adaptive response
  • Direct response for host defence = Phagocytosis and Antimicrobial activity
74
Q

Why would people with HIV/Aids be susceptible to getting fungi diseases?

A

Due to their impaired immune system

Immunocomprimised

75
Q

What are some common yeasts?

A
  1. Candida species
  2. Cryptococci
  3. Trichosporon

(these are common members of the normal flora as well as cause of invasive disease)

76
Q

What are some common moulds?

A
  1. Aspergillus
  2. Fusarium
  3. Scedosporium apiospermum

(these are common contaminants as well as cause invasive disease)

77
Q

What are some dimorphic fungi?

A
  1. Blastomyces
  2. Coccidiodes
  3. Histoplasma
78
Q

What do T cells recognise?

A

Proteins

79
Q

What do innate reponses recognise?

A

Foreign sugars

80
Q

What do acquired responses recognise?

A

Specific antigens

81
Q

What do most immunocomprimised individuals possess?

A

Most immunocomprimised individuals will be asymptomatic

82
Q

What are some non-cellular immune defences?

A
  • Skin, mucous membrane
  • Secretions
  • Microbial
    antagonism
83
Q

What are some cellular immune responses?

A
  • Innate cells, neutrophils
  • Inflammation (cytokines)
  • Phagocytosis (macrophages)
  • Host defence peptides
  • Complement
  • Nutritional immunity
84
Q

What are some antigen-specific immune responses?

A
  • Humoral (B cells, antibodies)
  • Cell mediated (T cell)
  • Memory responses
85
Q

How do yeasts enter?

A

From the drying of mucous membranes

86
Q

What does the immune response see?

A

Candida albicans - They see mannoprotein fibrils

Aspergillus fumigatus - Fibril free

Cryptococcus neoformans - Elaborate capsule

87
Q

What are some pattern recognition receptors?

A

CLR (C type lectin receptors)

NLR (NOD like receptor)

TLR (Toll like receptors)

88
Q

What do CLR recognise?

A

The sugars on the surface of the fungi

89
Q

What is CARD9?

A

It is a signalling pathway for fungi

90
Q

What do dectins do?

A

They recognise sugars on the surface of the molecule

91
Q

What does tissue damage do?

A

It starts up the system to repair the tissue

92
Q

What does hypha do?

A

It produces candidalysin which causes pores. Calcium flux goes in and out of the cell. LDH goes out of the cell. Goes from being a normal structural tissue to be a stimulating tissue

93
Q

What do people with CARD9 deficiency have?

A
  • Invasive fungal diseases
94
Q

What do people with Chronic mucotanenous candiosis (IL-17) deficiency have?

A
  • Defects in 1L-17 pathway
95
Q

What does absence of IL-17 result in?

A

In fungal disease

96
Q

In PAMP, how is downstream signalling initiated?

A

Dectin-1, Dectin 2-3, and Muscle-Dectin-3 heterodimers couple with immunoreceptor tyrosine based activation motif (ITAM) and Fcr-y associated ITAM motifs

97
Q

What does downstream signalling lead to?

A

Reactive oxygen speicies (ROS) production and caspase activation and recruitment domain containing protein 9 (CARD9)

98
Q

How is pro-IL-1B and pro-IL-18 cleaved?

A
  1. Bcl-10/MALT1 complex-mediates activation of NF-κB pathway.
  2. ROS triggers NLRP3 inflammasome assembly and activation
  3. This cleaves pro-IL-1β and pro-IL-18 into mature forms to elicit protective roles in anti-fungi immunity
99
Q

What does the Th1 IFNg maintain?

A

Th1 IFNg maintains mononuclear inflammation protects against Candida albicans, Histoplasma capsulatum, Cryptococcus neoformans, and Aspergillus fumigatus

100
Q

What does the Tfh provide help for?

A

Tfh provides help for B cells, Ig class switching and affinity maturation

101
Q

What does the Th17 IL-17 recruit?

A

Th17 IL-17 recruits neutrophils protective against Candida albicans, Histoplasma capsulatum and cocciodes

102
Q

What are Tregs important function?

A

Important in most fungal infections

103
Q

What does Th2 protect against?

A

Th2 protective against Pneumocystis
Detrimental for protection against Candida albicans, Histoplasma capsulatum, Cryptococcus neoformans, and Aspergillus fumigatus

104
Q

What happens to the skin, intestines, and lungs to humans with the excessive inflammation from the IL-17 in fungal disease?

A

Skin - Psoriasis

Intestines - IBD

Lungs - Asthma and COPD

105
Q

TRUE OR FALSE? Most pathogen attacks are NOT contained early before adaptive immune responses are required?

A

FALSE

Pathogen attacks ARE contained before adaptive immune responses are required

106
Q

What are protein cascades?

A

They play a crucial role in innate immunity

107
Q

What are the response times for innate, early induced and adaptive immunity?

A

Innate - 0-4 hours

Early induced - 4-96 hours

Adaptive - More than 96 hours

108
Q

What are defensins?

A

First line of defence

They are antimicrobial peptides of innate immunity

109
Q

What are some examples of intracellular organisms?

A

Leishmania spp

Cryptococcus neoformans

110
Q

Where do lamellar bodies sit on the skin?

A

In the stratum granulosum

Eukaryotic Microbio (4 decks)

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