Unit 7: Parasite Infections Flashcards

1
Q

what makes parasites living in the skin (such as bot fly larvae) successful?

A

it is an area of low immune surveillance and they only persist for a short amount of time

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2
Q

what does the blood brain barrier reduce/prevent?

A

trafficking of some immune cells, prevents antibodies reaching the brain

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3
Q

how do antibodies kill/affect/interact with parasites?

A
  • neutralization of essential antigens
  • activation of MAC complement cascade (lyse targets and C3b)
  • act as opsonin’s
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4
Q

What expresses IgG?

A

phagocytes (neutrophils, macrophages)
isotypes have different properties

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5
Q

What expresses IgE?

A

eosinophils, basophils, mast cells (absorbed onto cells before interaction with antigen)

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6
Q

how is IgM produced?

A

by naive B cells on first contact
followed by: helper T cell (CD4) bind MHC II (cytokine production) -> memory cells + plasma cells (IgG, IgA, IgE)

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7
Q

What is different about IgA?

A

only found on mucosal surfaces, eg, is normally secreted into the intestines

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8
Q

what is steric interference? give an example

A

natural antibodies block neutralising antibodies
plasmodium infection natural antibodies can stop monocloncal antibodies which are designed to block erythrocyte invasion -> eg, IgM bigger molecule than the more ‘effective’ IgG

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9
Q

what factors control antibody production?

A

T cell cytokines -> Th1/2

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10
Q

examples of Th2 responses

A

increase production of IL-3-6,10
help B cells produce antibodies via proliferation and isotype switching
IL-5 = IgE production

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11
Q

examples of Th1 responses

A

increase production of TNF and gamma interferon
help cell-mediated immune responses via macrophage and cytotoxic T cell recruitment

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12
Q

name the stage specific antigen seen on sporozoites

A

circumsporozoite protein (CSP) - not seen in blood or sexual stages

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13
Q

mechanism behind ‘smokescreen’ effect in eg, trypanosomes

A

VSG released from surface by phospholipase C (antibody binding action)
soluble VSG competes with VSG = antibody incapacitation

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14
Q

how do antigens with repeating epitopes affect host immune response?

A

cross-linkage on B cell surface receptor = B cell proliferation + IgM expression = less effective clearance
resistance to T cell signals that cause isotype switching/ affinity maturation

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15
Q

What is effective at clearing extracellular parasites?

A

IgE
BUT
can coat exterior with glycans, stimulate Th1 response or non-specific IgE absorption onto FcE (cross-linkage interference)

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16
Q

advantages of hiding in erythrocytes?

A

no nucleus - limited invasion response
no intracellular killing mechanisms
don’t express MHC I (cant present antigen)

17
Q

how do macrophages kill intracellular parasites?

A

PRRs
phagocytosis
anti-microbial peptides
lysosomal enzymes

18
Q

different Th responses?

A

IL-12 production (macrophage) = naive T cell develop into Th1
Th1 = activation of phagocytosis
(Th2 doesn’t help clear intracellular)

19
Q

how does leishmania modify Th responses?

A

selective inhibition of IL-12 = reduction of Th1 production
stimulation of IL-10 production = reduce MHC II, increase Th2 cell = suppression of macrophage function