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Parasitology > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

What causes Th0 cells to become Th1 cells?

A

IL-12

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2
Q

IL-12 is produced by?

A

Antigen presenting cells such as macrophages

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3
Q

What causes macrophages to become classically activated?

A

Direct activation: T cell CD40L binds CD40 on the macrophage

Indirect activation: IFN-g

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4
Q

Indirect classical activation of macrophages?

A

Cytokine IFN-g

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5
Q

Direct classical activation of macrophages?

A

CD40L binding to macrophage CD40

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6
Q

What cytokine leads to classical activation of macrophages?

A

IFN-g

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7
Q

What cytokine leads to alternative activation of macrophages?

A

IL-4

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8
Q

Alternative macrophage activation can also be known as?

A

Wound healing

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9
Q

Which cytokine leads to deactivation of macrophages?

A

IL-10

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10
Q

What causes Th0–>Th2?

A

IL-4

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11
Q

What causes Th0–>Th1?

A

IL-12

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12
Q

What are the roles of dendritic cells?

A

Antigen presenting cells

IL-12 producing

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13
Q

CD8+ cell importance?

A

Produce IFN-g which can classically activate macrophages

Can kill infected cells directly via perforin and granzymes

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14
Q

CD4+ cell importance?

A

Produce IFN-g which can classically activate macrophages
Can activate naive B cells causing them to become antibody producing plasma cells
Treg
Produce IL-10 to regulate the immune response

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15
Q

In which infections are CD8+ cells more important?

A

When cells are infected
Intracellular parasites
Can use granzymes and perforin
Can produce IFN-g

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16
Q

In which infections are CD4+ cells more important?

A

Blood stage infection
When the parasites are extracellular- can be opsonised by antibodies
IFN-g is produced

17
Q

Which T cell is most important during the liver stage of Plasmodium infection and why?

A

CD8+

Can kill infected liver cells via perforin and granzymes

18
Q

Which T cell is most important during the blood stage of Plasmodium infection and why?

A

CD4+ T cells

Lead to antibody production, which can opsonise the infected RBCs or extracellular merozoites

19
Q

CD8+ cells and cerebral malaria?

A

CD8+ T cells can cause severe cerebral malaria through accumulation in the brain, destruction of the blood brain barrier and excessive inflammation

20
Q

Which T cell type is more important in Leishmania infection and why?

A

CD4+

Leishmania is present in macrophages and therefore cannot be accessed by CD8+ T cells

21
Q

Why are CD8+ T cells not important in the blood stage of malaria?

A

RBCs do not possess MHC-I

Therefore antigen cannot be expressed

22
Q

Why are CD8+ T cells not important in T.brucei infection?

A

As it is an extracellular parasite

23
Q

What is IL-10?

A

Anti-inflammatory cytokine

24
Q

When IL-10 is depleted it leads to?

A

Increased reduction in parasite load

25
Q

However, why is it not a good idea to drastically deplete IL-10?

A

As IL-10 is important in regulating the immune response, depleting IL-10 leads to increased pathology associated with the disease

26
Q

What else can regulate the immune response?

A

Tregs

27
Q

What are Tregs?

A

A subset of CD4+ T cells which can produce IL-10, prevent self-reactive T cell proliferation and can regulate the immune response

28
Q

What does IL-10 do to macrophages?

A

It deactivates them

29
Q

Removal of IL-10 and Tregs can lead to?

A

Reduced parasite load

Increased pathology associated with the disease

30
Q

How do CD4+ cells activate naive B cells?

A

CD40L on the T cell binds the CD40 on the B cells and causes them to become plasma cells

31
Q

What are the roles of antibodies?

A
  • Neutralise parasites, preventing cell entry
  • Opsonise parasites for phagocytosis
  • Activate classical complement
  • Cause the membrane attack complex to form
  • ADCC: Antibody dependent cell mediated cytotoxicity via NK cells
  • Binding action alone can cause cell rupture
32
Q

How can Leishmania interfere with interferon signalling?

A

Interferes with the JAK/STAT pathway

33
Q

Evasion of CD8+ cells?

A
  • T.brucei extracellular
  • Giardia extracellular
  • Leishmania within macrophages
  • Blood stage Plasmodium is within erythrocytes which do not express MHC-I
34
Q

Evasion of CD4+ cells?

A
  • T.brucei antigenic variation and coat cleaning mechanism
  • Plasmodium antigenic variation
  • Giardia antigenic variation
  • Plasmodium rosetting
  • Intracellular parasites: Toxoplasma, T.cruzi, Leishmania,, Plasmodium
  • VSG coat of T.cruzi hides the invariant surface receptors
  • Flagellar pocket of the kinetoplastid protozoa shelters invariant receptors
35
Q

Evasion of NK cells?

A
  • T.brucei is extracellular

- Giardia is extracellular

36
Q

Evasion of complement?

A
  • LPG of Leishmania can prevent MAC
  • GP63 of Leishmania converts C3b to iC3b
  • Trans-sialidase of T.cruzi transfers host sialic acid to mucins on the cell surface
  • Intracellular parasites
  • T.brucei dense VSG coat prevents complement mediated lysis
37
Q

Evasion of interferons?

A

Leishmania can prevent interferon JAK-STAT signalling

38
Q

Evasion of innate immunity?

A
  • Leishmania LPG can delay the fusion of the phagosome with the lysosome to allow time for the promastigotes to differentiate into amastigotes
  • Leishmania can survive in the phagolysosome and can even replicate here
  • Leishmania can induce the macrophage or produce its own arginase which can deplete the level of L-arginine available for use by iNOS- inducible nitric oxide synthase to produce nitric oxide
  • T.cruzi escapes the acidification of the phagosome by entering the cytosol and replicating there, this is facilitated by the trans-sialidases and by haemolysins which are pore forming
  • Entering a dormant state in cells can help to evade the immune response e.g. Toxoplasma bradyzoites are immunologically dormant and can go undetected
  • Intracellular parasites can avoid being phagocytosed as they are intracellular

Parasitology (17 decks)

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