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PHS 932 > Block 2 Lecture 4 -- Parasites > Flashcards

Block 2 Lecture 4 -- Parasites Flashcards

1
Q

What are types of parasites?

A

1) protozoa
2) helminths
3) ectoparasites

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2
Q

Why are parasites problematic?

A
    • evoke weak innate immune response

- - mechanisms of evasion

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3
Q

How do parasites resist the innate response?

A

1) some too large for phagocytosis
2) replicate and resist degradation within phagocytes
3) penetrate through skin

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4
Q

How many species of leishmaniasis?

A

20

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5
Q

What are the types of leishmaniasis?

A

1) cutaneous
2) mucocutaneous
3) visceral

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6
Q

Characterize cutaneous leishmaniasis

A

bad - scars

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7
Q

Characterize mucocutaneous leishmaniasis?

A

2nd worst form - ulcers

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8
Q

Characterize visceral leishmaniasis

A

worst form - death

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9
Q

What is the tx for leishmaniasis?

A

amboB/amBisome

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10
Q

Th1 overactivation =

A

pro-inflammatory diseases

– T2DM, GVHD, arteriosclerosis

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11
Q

Th2 overactivation =

A

anti-inflammatory Ab-mediated diseases

– infection, allergy, autoimmunity

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12
Q

What is the signature cytokine of the Th1 response?

A

IFN-gamma

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13
Q

What is the signature cytokines of the Th2 response?

A

IL-4

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14
Q

What is classical macrophage activation?

A

enhanced killing induced by IFN-gamma

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15
Q

What is alternative macrophage activation?

A

tissue repair stimulated by IL-4 and IL-13

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16
Q

What are the results of Th1 immune response?

A

1) classical macrphage activation
2) complement binding
3) IgG

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17
Q

What are the results of Th2 immune response?

A

1) Ab production
2) mast cell degranulation
3) intestinal mucous secretion and peristalsis
4) eosinophil activation
5) alternative macrophage activation

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18
Q

What causes opsonization in Th1?

A

IFN-gamma – IgG

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19
Q

What causes complement activation in Th1?

A

IFN-gamma – IgG

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20
Q

What causes classical macrophage activation in Th1?

A

IFN-gamma (from Th1 CD4, Treg and NK)

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21
Q

What causes Th1 differentiation/proliferation?

A

IL-12 (from macrophages, DCs) stimulates T cell to make IFN-gamma to cause feedback

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22
Q

What causes Th2 differentiation/proliferation?

A

IL-4 (from mast, eosinophils) stimulates T cell to make IL-4 to cause feedback

23
Q

What causes alternative macrophage activation?

A

IL-4 and IL-13

24
Q

What causes intestinal mucous secretion and peristalsis?

A

IL-4 and IL-13

25
Q

What causes activation of eosinophils?

A

IL-5

26
Q

What causes production of IgE?

A

IL-4 targeting B cells

27
Q

What causes mast cell degranulation?

A

recognition of epsilon receptor of IgE

28
Q

What cytokines do Th2 CD4’s produce?

A

IL-4, IL-5, IL-13

29
Q

What cytokines do Th1 CD4’s produce?

A

IFN-gamma

30
Q

What do Tfh cells in Th1 produce?

A

IFN-gamma

31
Q

What do Tfh cells in Th2 produce?

A

IL-4

32
Q

How are helminths that are too large to be phagocytosed eliminated?

A

1) IgE binds

2) mast cell degranulates

33
Q

What component (Th1/Th2) has best ADCC?

A

Th2

34
Q

What other Abs are involved in Th2?

A

IgA and IgG

– both bind helminth to activate eosinophil degranulation

35
Q

How is IgA production stimulated?

A

TGF-beta

36
Q

How is IgG production stimulated?

A

IFN-gamma

37
Q

What immune response is required to fight trypanosomiasis and why?

A

Th2…trypomastigotes injected in bloodstream are never phagocytosed

38
Q

What are the hosts in trypanosomiasis?

A

tsetse fly + human

39
Q

Common name for trypanosomiasis?

A

african sleeping sickness

40
Q

What are the hosts in leishmaniasis?

A

female sandfly + mammals

41
Q

What are the stages of infection in malaria?

A

1) sporogonic
2) exo-erythrocytic
3) erythrocytic

42
Q

What is the sporogonic cycle in malaria?

A

mosquito stages, plus when mosquito injects sporozoites into human

43
Q

What is the exo-erythrocytic cycle in malaria?

A

1) injected sporozoites infect hepatocyte
2) form intracellular schizont
3) schizont ruptures and invades blood

44
Q

What is the erythrocytic cycle in malaria?

A

1) schizont infects RBC
2) trophozoite matures and ruptures
2) trophozoite forms gametocytes to be ingested by mosquito

45
Q

What organism is involved in hookworm?

A

Filariform larvae

46
Q

What are the stages of infection of hookworm?

A

1) infective: enters through unbroken skin, migrates to intestine
2) diagnostic: eggs spread in feces

47
Q

Describe the infection stages in leishmaniasis.

A

1) promastigotes invade macrophages, granulocytes, or are phagocytosed
2) multiply into amastigoes
3) leave and infect other cells

48
Q

How does leishmaniasis evade the immune system?

A

1) alters complement system
2) avoid innate mechanisms
3) modulate cytokines
4) inhibit Ag-presentation and T activation
5) alter T-cell differentiation

49
Q

How does leishmaniasis alter the host complement system?

A

phosphorylates complement proteins

sheds MAC

50
Q

How does leishmaniasis avoid innate mechanisms?

A
    • inhibits formation of phagolysosome
    • scavenges ROS
    • inhibits enzymes
51
Q

How does leishmaniasis modulate cytokines?

A
  • suppresses activating cytokines

- induces inhibitory cytokines

52
Q

How does leishmaniasis inhibit antigen presentation/T activation?

A
    • suppresses MHC class II expression
    • inhibits p-MHC formation
    • downregulates B7
53
Q

How does leishmaniasis alter T-cell differentiation?

A

induces Th2 response

PHS 932 (23 decks)

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