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Case 9 > Immunology 1 > Flashcards

Immunology 1 Flashcards

1
Q

What mechanical barriers protect against infection by viruses?

A
  • Epithelial cells joined by tight junctions
  • Longitudinal flow of air or fluid
  • Movement of mucus by cilia
  • Tears
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2
Q

What chemical barriers protect against infection by virus?

A
  • Fatty acids
  • Low pH
  • Antimicrobial enzymes
  • Pulmonary surfactant
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3
Q

What is the cytolytic action of influenza?

A

Influenza causes acute cell death of ciliated resp epithelial cells + removes mucus-secreting cells + blocks function of muco-ciliary escalator

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4
Q

What are the layers of defence?

A
  1. Immediate innate
  2. Induced innate
  3. Adaptive
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5
Q

How long is immediate innate immunity?

A

0-4 hrs

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6
Q

How is the virus recognised in immediate innate immunity?

A
  • Soluble effector molecules = defensins, lactoferrin + lysozyme
  • Resident effector cells in infected tissue = macrophages, mast cells + cDc’s + some memory T cells + NK cells
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7
Q

How long is induced innate immunity?

A

4 hrs - 4 days

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8
Q

What are the sentinel cells of the body and what is their role?

A

= macrophages, dendritic cells, few NK cells + v few memory type lymphocytes

Detection

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9
Q

What are Langerhan cells?

A

Distinct sub population of self-renewing DC’s

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10
Q

Where can viruses uncoat and where do PRR’s exist?

A

Plasma membrane + within endosomes

TLRs 3, 7, 8, 9 = located in endosomes

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11
Q

3yo with high fever, right sided tonic-clonic seizures + paralysis right face + arm
MRI - lesions in left parietal lobe + left thalamus
WBC - 180 (normal <5), 97% lymphocytes
PCR - HSV-1 in CSF
History - viral encephalitis at 6 mo

What is the diagnosis?

A

Recurrent herpes simplex encephalitis

Associated with genetic defects in TLR-3 signalling pathway + failure of neurones to produce type 1 interaction

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12
Q

Where is the primary site of infection for HSV-1?

A

Oral mucosa

Then transported through sensory neurones > trigeminal nerves + ganglia where it establishes latent infection

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13
Q

What are the consequences of triggering TLRs?

A

Communication

Macrophages produce range of cytokines upon sensing virus

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14
Q

18 yo male
Pyrexia, persistent pharyngitis + cervical lymphadenopathy

What is the diagnosis?

A
  • EBV
  • Gains entry to tonsillar B lymph + replicates rapidly
  • EBV virions pass via afferent lymphatics into cervical nodes
  • Causes B lymph prolif > CTL kill infected B cells > symptoms
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15
Q

What are the classic signs of viral infection?

A 
Malaise 
Sleepiness 
Myalgia 
Loss of appetite 
Chills + fever
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16
Q

What cytokines do macrophages produce in response to virus?

A
  • Pyrogenic cytokines - act on hypothalamus to increase body temp, act on muscle to increase fat + protein utilisation
  • IL-1 & IL-6 = endogenous pyrogens + can actually cross into hypothalamus + bring about PGE2
  • PGE2 production = innervation of sympathetic system = shivering, non-shivering thermogenesis + skin vasoconstriction
17
Q

What are interferons?

A

Class of cytokines which defend against viral infections

18
Q

What interferons are capable of producing interferons alpha and B and how?

A
  • All cells
  • Interferon response activates NK cells to kill virus-infected cells
  • Cause systemic symptoms associated with viral infections
  • IF alpha + beta = induced + released within hours of infection
19
Q

How to TLR’s lead to transcription of type 1 IFNs alpha + beta genes?

A
  • Interferon response factors phosphorylated

- Then enter nucleus to initiate interferon mRNA synthesis

20
Q

What is the role of interferon stimulated genes (ISGs)?

A
  • Suppress viral entry, viral replication + alter cellular metabolism to generate anti-viral state
  • Virus detected by PRRs > activation IRFs > enter nucleus + initiate transcription of IF alpha + beta
  • These bind to IFN receptors to trigger JAR/STAT activation > transcription ISGs
21
Q

How do IFNs protect neighbouring cells?

A

Induce antiviral state in neighbouring uninfected cells

22
Q

What does the cytosolic detection of viral infection by PRRs (RIG like receptors) lead to?

A
  • RLRs enable cells to make type 1 interferon
  • Many viruses infect cells by direct membrane fusion
  • Host cell evolved PRR’s to detect viral nucleic acids in cytosol
  • RLR’s detect abnormal RNA molecules + trigger response
23
Q

What effect do most pathogenic viruses e.g. ebola have on the antiviral state?

A

Shut off supply of IFNs + prevent antiviral state

24
Q

What is the role of plasmacytoid dendritic cells (pDCs)?

A
  • Increase capacity for producing IFNS alpha
  • Mainly in blood + lymphoid tissues
  • Significant during viraemia
  • Express high levels of TLRs 7 + 9
25
Q

What is the role of conventional dendritic cells (cDCs)?

A
  • Activation of naive T cells

- Localised in peripheral tissues in absence of infection

26
Q

Why not administer measles, mumps + rubella vaccines singly and a week apart?

A
  • Interferon response to 1st vaccine would suppress replication of 2nd and therefore diminish immune response to 2nd
  • Immune response to 1 live virus vaccine might be impaired if administered within 30 days of another
27
Q

How do NK cells detect changes at surface of infected cells?

A
  • Combination of activatory + inhibitory receptors found on NK cell surface
  • Triggering of NK cells dependent on balance of receptors
28
Q

How do NK cells kill virally infected cells?

A

Release of perforins + granzymes that perforate membranes of target cells + induce caspase mediated death

29
Q

Describe the kinetics of immune response to viral infection

A
  1. Production of IFN-alpha & beta, TNF-alpha and IL-2
  2. NK cell killing of infected cells
  3. T cell killing of infected cells

Case 9 (11 decks)

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