Integrated response to infection Flashcards

(37 cards)

1
Q

Immune response is d_______ and d_________

A

dynamic
diverse

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2
Q

What are the four stages for sterilisation of pathogen

A
  1. Establishment of infection
  2. Inductive phase
  3. effector phase
  4. memory phase
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3
Q

Establishment of infection

A

innate immune cells recognise non-self antigens

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4
Q

Inductive phase [2]

A

cells become activated
differentiate in lymph node

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5
Q

Effector phase

A

enter adaptive immune system (B and T cells)

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6
Q

Memory phase [2]

A

effector function silenced
memory cells made

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7
Q

Describe type 1 effector function [3]

A
  • Th1 produces IGN-y
  • activates macrophages
  • target intracellular pathogens
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8
Q

Describe type II effector function [3]

A
  • Th2
  • produces cytokines
    activates eosinophils, basophils and mast cells
  • target extracellular pathogens
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9
Q

Describe type III effector function [3]

A
  • Th17 produces IL-17 and IL-22
  • activates neutrophils
  • target extracellular pathogens and fungi
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10
Q

Define the term opportunist infection [3]

A
  • lots of bacteria on the skin
  • do not penetrate skin or cause infection
  • until there is an opportunity (abrasion)
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11
Q

Define the term acute infection [2]

A
  • quick replication and spreading to new host
  • before immunological response
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12
Q

Define the term chronic infection [2]

A
  • persisting long term
  • avoiding elimination
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13
Q

Identify complicating factors [3]

A
  • numerous developmental stages
  • numerous hosts
  • many environments
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14
Q

What is meant by absence of sterilising immunity [1]

A

Body is unable to get rid of parasite entirely

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15
Q

Why are parasites harder to eliminate than bacteria?

A
  • eukaryotes
  • more like human cells
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16
Q

Describe the leishmania species [5]

A
  • host is sandfly
  • draws blood which transfers pathogen
  • various species
  • gives rise to different types of diseases
  • invades macrophages through phagocytosis
17
Q

Describe the role of neutrophils in the immune response to leishmania parasite [3]

A
  • netosis: limit mobility
  • activate macrophages, activating the adaptive immune response
  • release CCL3 activating dendritic cells
18
Q

Describe the adaptive immune response to the leishmania parasite(Th cells) [3]

A
  • Monocyte derived macrophage to lymph node
  • releases IL-12
  • causes Th0 cells to differentiate into Th1 cells
19
Q

Would mouse A (Th1 cell) or mouse B (TH2 cell) be best suited for killing the leishmania. Why?

A
  • Mouse A
  • Th1 invovled in activates macrophage action
  • key in the immune response to leishmania
20
Q

Describe the schitosoma parasite? [3]

A
  • parasitic worm
  • infection in the intestine
  • infected snails that bite and infect humans
21
Q

Briefly describe the lifecycle of the schitosoma [5]

A
  • penetrates across unbroken skin
  • locates blood capillaries
  • feeds on blood, and carried by flow
  • males and females pair
  • females release eggs
22
Q

Identify how the parasite can be diagnosed [5]

A
  • enlarged liver/spleen
  • blood in urine
  • eggs in stool
  • IgM/IgG count high
  • DNA from worms (PCR)
23
Q

What is another word for parasitic worm [1]

24
Q

Would mouse A (Th1 cell) or mouse B (TH2 cell) be best suited for killing the schitsosoma. Why?

A
  • Mouse B would be best
  • immunity relies on Th2 cells
25
What interleukins does the Th2 cell release and what is their role [9]
- IL12: cell repair and increased mucous - IL-13: increased smooth muscle contractibility to expel worm - Produce Il-5: recuit and activate eosinophils - Produce IL-3 and IL-9: mast cell recruitment
26
What is a granuloma?
cluster of leukocytes
27
What is calcification
tissue hardening
28
What is fibrosis
tissue thickening/scarring
29
What cell is essential for the forming of granulomas?
macrophages
30
Describe the difference between granulomas in an acute vs chronic infection [1]
In chronic infections cells (and tissues) are more organised
31
What is the role of granulomas in terms of egg elimination
- facilitate the release of eggs
32
Suggest why it is difficult to to design fungal drugs. [2]
- eukaryotic cells, similar to self cells - hard to kill fungus without damaging surrounding tissue
33
How can mycosis be divided. Which is most dangerous [5]
- according to the body part it infects - superficial - subcutaneous - systemic (danger)
34
How does COVID-19 fungal infection counts.[2]
- increase as it surpasses the immune system - secondary infarction
35
Describe the Candida family [2]
- fungus colonises normal oral, GI and urogenital mucosa - disrupts mucosal barriers leads to persists superficial infection
36
Describe the role of Dectin-1 in the recognition of fungal infections [4]
- highly expressed on dendritic cells - has C-type lectin carb recognition domain - recognises glucans on fungi surface - when engaged DECTIN-1 leads to production of inflammatory cytokines and ROS
37
What does the immune system recognise on fungi? [3]
- conserved cell constituents - glucans mannas - galactins