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Biology Of The Immune System > L8&9 : Immune responses against bacterial infections > Flashcards

L8&9 : Immune responses against bacterial infections Flashcards

1
Q

What factors affect the type of effector mechanism required in an immune response?

A

Type of pathogen, localisation, challenge and site of infection

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2
Q

Compare innate and adaptive immune mechanism

A
  • innate are non specfic and fast acting, while adaptive are specific and take longer to develop
  • adaptive exhxibits memory but innnate doesn’t
  • innate uses physical barriers, component system, phagocytes and NK cells, while adaptive uses Abs and cell mediated immunty
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3
Q

What role do innate defence mechanisms have?

A

Act as first line of defence but are ineffective against many pathogen

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4
Q

What role do adaptive defence mechanisms have?

A

They enhance and focus innate defences, and are less easily evaded by pathogens

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5
Q

Name the types of specific response CD4+ cells

A

Th1,2 & 17

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6
Q

What is the function of Th1 cells?

A

Active against intracellular pathogens

- activates macrophages and stimulates CD8+ cells

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7
Q

What is the function of Th2 cells?

A

Active against extracellular pathogens

  • supports Ab production, particularly class switching to IgE
  • activates esinophils, basophils and mast cells
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8
Q

What is the function of Th17 cells?

A

Active against extracellular bacteria& fungi

  • important in attracting inflammatory cells e.g. neutrophils
  • induced early in infection
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9
Q

What innate responses can cell wall components (e.g. LPs, peptidoglycan) induce?

A

The binding to Toll-like receptors (TLR) on macrophages

  • there are 10 TLR genes in humans: receptors recognise distinct molecular patterns on microbes, located on plasma membrane & endocytic vesicles
  • NOD like receptors
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10
Q

The binding of PAMPs to TLRs can cause what responses?

A
  • promotion of inflamaation
  • promotion of dendritic maturation
  • influence differentiation of T cells
  • activation of B cells (TI-1 Ags)
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11
Q

Why is phagocytosis often effective against bacteria?

A

Bacteria may have protective capsules but can be opsonised by Ab/ componenet

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12
Q

What is the role of Abs in bacterial infection

A
  • opsonisation: binds Fc receptors on phagocytes
  • componenet activation: promotes inflammation via C3a + C5a, opsonise by binding C3b receptors on phagocytes & lysis of gram -ve organisms
  • bind and neutralise toxins e.g. tetanus, diphtheria
  • bind to surface structures to prevent mucosal adherance
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13
Q

What is a conseqeunce of defects in terminal complement componenets?

A

Can lead to susceptibility to Neisseria spp. and bacterial cell division becomes more vulnerable (can lead to cell death)

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14
Q

Gram +ve bacteria can be killed by lysis. True or false

A

False, gram -ve bacteria are killed by lysis

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15
Q

Some bacteria survive within phagocytes. True or false?

A

True

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16
Q

Give an example of how outcome of infection depends on the type of response

A

e. g. Myobacterium leprae
- tuberculoid leprosy: strong Th1 repsonse, few live bacteria, slow progessino, granuloma formation
- lepromatous leprosy: strong Th2 and Ab response, large no bacteria in macrophages, disseminated infection and can be fatal

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17
Q

What mechanisms are uesd to protect against extrcalleular pathogens and intracellular organisms respectively?

A
  • Abs are imporant for extracellular pathogens e.g. s. pneumoniae
  • T cell effector mechanisms are important for intracellular organisms e.g. mycobacterium
18
Q

How do virus infected host cells use type-1 interferons (IFN alpha & beta)?

A

1- induces resistance to viral replication in all cells, by inducing Mx proteins, 2’-5’ linked adenosine ogliomer and the kinase PKR
2- increase MHC class I expression and Ag presentation in all cells
3- activates dendritic cells and macrophages and NK cells to kill virus infected cells
4- induces chemokines to recruit lymphocytes

19
Q

IFN can induce the synthesis of what 2 molecules?

A

Protein kinase and 2’5’- oglioadrenylate synthetase

20
Q

How can IFN lead to the degradation of viral mRNA?

A

IFN induces the synthesis of 2’5’ oglioadenylate synthetase

  • leads to adenine trinucleotide being synthesised
  • this activatees endonuclease
  • viral mRNA degraded
21
Q

How can IFN lead to the inhibition of protein synthesis?

A

IFN induces protein kinase

  • leads to phosphorylation and inactivation of eIF-2
  • this inhibits protein synthesis
22
Q

At which point of infection can type I interferons be seen?

A

In early responses

23
Q

What are type II interferons (IFN gamma) secreted by?

A

Activated T and NK cells

24
Q

How do type II intereferons respond to infection?

A
  • inhibit Th2 response (Ab)
  • promotes Th1 (cell killing)
  • recruits macrophaages (driving Th1 response)
25
Q

rIFN alpha can be used to treat what diseases?

A

Hep B and C, and some cancers but side effects can be very severe

26
Q

What is the function of NK cells in the immune response

A
  • recognise structures on viral infected cellls & stressed in absence of Igs and MHC
  • kills by extracellular mechanism: perforin and granzyme (potent) so work fast
27
Q

How do NK cells distinguish between infected and uninfected cells?

A
  • Activating receptors: recognise carbohydrate ligands, triggers killing
  • Inhibitory receptors: recognises MHC class I molecules (no binding, only TCR can do this) and inhibits the activities & activation of these NK cells
28
Q

How do some viruses make cells more susceptible to NK killing?

A

By reducing MHC expression

29
Q

Explain methods of cell mediated specific immunity

A
  • CD8+ cells (CTL): recognises viral peptide and MHC class I

- cytokines with anti viral activity: e.g. IFN gamma (class II, helps activate macrophages)

30
Q

Explain the mechanisms by which CD8+ cells kill

A
  • secretion of cytotoxic granulese e.g. perforin which polymerises in membrane, grnazymes (proteases) which enter cell
  • Fas ligand on T cell interacts with Fas on target
31
Q

What 2 processes/ interactinos lead to specific recognition?

A

Collision+ non specific adhesion

32
Q

How does collision and non specific adhesion lead to specific recognition?

A
  • redistributes cytoskeleton and cytoplasmic components of T cells
  • leads to release of granules (vesicles) at site of cell contact
  • this method is powerful and targeted, causing the polarised release of granules
33
Q

How to CTLs kills cells?

A
  • recognise and bind virus infected cell
  • programs target for death, including DNA fragmentatino
  • CTL migrates to new target
  • target cell dies by apoptosis
34
Q

How do CTLs secrete cytokines?

A
  • inhibit viral replication
  • upregulate MHC class I and II expression & Ag presentation
  • increases macrophage phagocytosis of dead cells
  • promotes NK cell killing activity
35
Q

How do Abs respond to viral infections?

A
  • Neutralises free virus (prevent entry into and spread between cells
    can prevent spread within body (e.g. poliovirus) or protect mucosal surfaces against reinfection (e.g. flu)
  • Opsonise to increase phagocytosis
  • Activate complement leading to lysis (enveloped virus)
36
Q

Explain the role of Abs in cell mediated immunity of influenza

A
  • infection induces Ab and CTL response
  • Ab recognises viral haemagglutinin and neruaminidase
  • high levels of CTL activity correlates with reduced viral stability
  • epidemics arise due to new strains not recognised by Ab
37
Q

How does HIV affect the immune system?

A
  • attacks specific immune system
  • targets CD4 T cells, macrophages and dendritic cells
  • progressive developments of AIDS leads to opportunistic infections
38
Q

How do Abs protect against parasites?

A

By opsonisation, complement lysis and ADCC (antibody dependent cell mediated cytotoxicity)

39
Q

What response can some helminths (worms) evoke?

A

Can induce strong IgE Ab response which leads to the activation of mast cells (mediated inflammation), eosinophils and ADCC

40
Q

What effector mechanisms are used for the malaria?

A

Different effector mechanisms are active at different stages

  • sporozoite and merozoite may be susceptible at Ab
  • Ab may also kill infected RBC
  • CTL active against infected liver cells

Biology Of The Immune System (9 decks)

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