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Pom > Immune Response To Infection > Flashcards

Immune Response To Infection Flashcards

1
Q

What are the 4 different pathogen niches during infection?

A
  • Extracellular e.g. Staphylococcus, Streptococcus, Candida, microbiota, worms
  • Surface adherent e.g. enteropathogenic & enterohaemorrhagic E. coli
  • Intracellular vacuolar (that occupy specialised compartment in host cell e.g. modified lysosome or ER) e.g. Salmonella, Chlamydia, Legionella, Coxiella, Plasmodium
  • Intracellular cytosolic e.g. viruses, Listeria, Bukholderia, Mycobacterium
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2
Q

How does an immune response to an infection start

A
  • Tissue damage (e.g. injury or by toxins produced by infectious agent)
  • Molecular detection of microbes- wrong thing in wrong place at wrong time
  • Then, intercellular communication happens e.g. interleukins
  • This leads to priming of the adaptive immune response
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3
Q

How does an immune response to infection end

A
  • Clearing infection
  • Stopping inflammatory cytokine production- more production of these can lead to tissue damage
  • Repairing tissue damage
  • Remembering the infection- immune memory
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4
Q

What are the 3 broad differences between innate and adaptive immunity?

A

Innate:

Fast acting

First line of defence

Germline encoded receptors

Adaptive:

Slower but long lasting

Variable receptors that mature over time

Also innate provides physical barriers whereas adaptive doesn’t.

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5
Q

Physical barriers provided by innate immunity

A

Skin,mucous,epithelial cells

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6
Q

Is complement part of innate or adaptive

A

Both

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7
Q

What are the key cellular components of innate immunity?

A

Neutrophils, macrophages, dendritic cells and natural killer (NK) cells

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8
Q

What are the key cellular components of adaptive immunity?

A

Cytotoxic T-cells, T helper cells, T regulatory cells, B lymphocytes and plasma cells

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9
Q

What is the difference in specificity between innate and adaptive?

A

Innate is less specific than adaptive as innate detects broad classes of pathogens via PAMPs (e.g. cell membrane components such as peptidoglycan) whereas adaptive can detect structural detail of antigens and may even recognise non-microbial antigens

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10
Q

Why is there greater diversity in adaptive immune receptors in comparison to innate immune receptors

A

Adaptive immune receptors are encoded by genes produced by somatic recombination hence they produce TCRs and Ig’s that have millions of different variations

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11
Q

List the general sequence of molecular and cellular events of an immune response?

A

Microbial molecules detected

Naïve host-cells are changed - gene expression leads to their activation

Production of antimicrobial molecules which send communication signals to alert neighbouring cells

Leads to the production of activated and specialised host cells

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12
Q

First responders to site of injury

A

Neutrophils are short lived~6 hours
Followed by monocytes that differentiate to become macrophages
Uncontrolled activity can lead to granulomas,excessive inflammation and tissue damage

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13
Q

How do phagocytes and other immune cells identify the class of pathogen?

A

Bacteria- typically cell wall components like LPS in E. coli

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14
Q

How does live vs dead bacteria elicit different immune responses?

A
    • Live E. coli elicits immune response-
      • inflammatory cytokines produced (e.g. IL-1beta that’s responsible for fever)
      • antimicrobial genes (that are directly toxic to bacteria)
      • metabolic genes (that help macrophage cope with these high, demanding jobs)
      • immunomodulatory genes (so that adaptive immune system appropriately primed)
    • Dead E. coli results in no immune response- macrophage tries to resolve inflammation rather than causing more
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15
Q

Cell surface molecules unique to fungi

A

Beta glucans

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16
Q

What type of immune response do fungi produce

A
  • Different kind of proinflammatory cytokines
  • Antimicrobial genes
  • Metabolic genes
  • Immunomodulatory genes
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17
Q

What type of immune response do viruses produce?

A
  • Interferon production that interfere with viral replication
  • Proinflammatory cytokines
  • Antiviral genes
  • ## Immunomodulatory genes
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18
Q

What do activated macrophages display

A

Phagocytosis and migration

Cytokine/chemokine production

Expression of cell surface molecules

Antimicrobial activity

Antigen presentation and T cell activation

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19
Q

What are interferons

A

Are special cytokines
Have direct antiviral activities
Detects viruses and gram negative intracellular bacteria

20
Q

3 types of interferons

A

Type I-IFN alpha/beta
Promotes antiviral response
Every primary infected cell can produce type I IFN

TypeII-IFN gamma
Only produced by lymphocytes
Promotes antibacterial immunity

Type III-lambda
Only produced at epithelial surfaces
Promote antiviral responses

21
Q

What are the immunomodulatory roles of IFNs?

A
  • Enhanced T-cell responses
  • Anti-inflammatory actions
  • Tissue repair
22
Q

How are virus infected cells killed

A

Cytotoxic T lymphocytes or natural killer cells

23
Q

2 anti microbial enzymes that are produced by a cytokine binding to a cytokine receptor

A

Phagocyte oxidase which produces reactive oxygen species

Inducibke nitric oxide synthase produces nitric oxide

24
Q

What are the soluble effector mechanisms of innate immunity?

A
  • Complement mediated bacterial destruction
  • Lectin-binding to neutralise cell attachment or entry
  • Iron chelation (siderophores) to prevent replication
  • Antibiotic-like peptides
25
Q

What are the cellular effector mechanisms of innate immunity?

A
  • Reactive oxygen and nitrogen radicals made by phagocyte oxidase and iNOS respectively- these genes never present in naive cells- only expressed when pathogen encountered
  • ## Acidification and digestion within phagosomes
26
Q

How are T cells activated

A

Activated macrophages and DCs present antigens in combination with MHC I and MHC II
Cytokines produced by apc produce suitable millieu for T cell activation eg IL12 promotes T cell replication
T cells provide cytokines that activate phagocytes eg IFN gamma upregulates MHC II expression for antigen presentation

27
Q

How are dendritic cells better able to respond to viral infections than macrophages?

A

Produce type I IFN

28
Q

How do T cells help B cells produce antibodies?

A
  • APCs become activated by infection and cytokines and present antigen to T cell which becomes activated to Th cell
  • Th cell helps activate the B cell with the correct BCR which produces antibodies against original antigen
29
Q

What are the 2 main T cell types?

A
  • Th1 cell (CD4 T cell) produced during bacterial infections that produce IFN-gamma and other cytokines that promote inflammation, phagocytosis and killing of microbes
  • Tc cell (CD8 T cell) produced during viral infections and will directly kill virus infected cells leading to apoptosis of the host cell, removing viral replicating niches
30
Q

What are some T cell functions

A
  • Phagocyte activation- T cell derived cytokines activate phagocytes which leads to enhanced killing of pathogens and more inflammation
  • Direct killing of infected cells- removal of replicative niches
  • B cell activation- antibody production and affinity maturation
  • Innate lymphoid cells (aka gamma delta T cells)- reside in mucosal surfaces and are a type of early responders to infection (act independently to MHC)
31
Q

Impact of age

A

Immune response gets weaker due to reduced thymic output

32
Q

What kind of genetic dysfunction leads to chronic granulomatous disease?

A

Loss of reactive oxygen soecies

33
Q

What genetic dysfunction leads to chediak higashi syndrome

A

Compromised lysosomes

34
Q

What genetic dysfunction is in immunosuppresion

A

Depletion/impairment of lymphocytes

35
Q

What kind of genetic dysfunction is present in HIV

A

Reduced CD4 T helper cells

36
Q

genetic dysfunction in the genes controlling what leads Severe Combined Immunodeficiency (SCID)?

A

Reduction of T and B cells

37
Q

What genetic disfunction leads to X-linked aggamaglobulinaemia?

A

Decreased serum IgG of all types

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38
Q

To which pathogens are Th17 made?

A

Fungi
Extracellular bacteria

39
Q

To which pathogens are Th1 made

A

Bacteria
Protozoa

40
Q

To which pathogens are Th2 made

A

Helminths
Allergens
Venom

41
Q

Intracellular pathogens

A

Macrophages are activated causing release of interferon gamma which causes T cells to differentiate into Th1
Excessive can cause autoimmunity and chronic inflammation

42
Q

Helminths

A

Causes mast cells and eosinophils to be activated which causes lease of IL-4,IL-5, IL-13. This causes T cells to differentiate into Th2
Excessive can cause allergy

43
Q

Extracellular bacteria and fungi

A

Causes neutrophil activation which causes release of IL-17 and IL-22. This causes T cells to differentiate into Th17

44
Q

PAMPs vs DAMPs

A

PAMPs are released by pathogens and are conserved structures eg bacteira have lps,fungi have beta glucan cell walls,viruses have surface glycoprotein

DAMPs are released by distressed or dying tissues recognized by ato released from dead cells,alarmins and some cytokines

45
Q

Apoptosis vs pyroptosis

A

Caspase 8,9,3,6,7

Caspase 1,4,5 for pyroptosis

46
Q

Phagocyte and T cell response

A

Intracellular pathogens cause macrophages to be activated causing release of IFN-gamma. Thus causes T cells to differentiate into Th1 cells. If left for too long it can cause autoimmune disease and chronic inflammation

Helminths activate eosinophils causing release of IL-4,5,13 which causes T cells to differentiate into Th2 cells. If left for too long ca cause allergy

Extracellular bacteria and fungi activate neutrophils to release IL-17,22 which activates Th17. If left for too long it causes autoimmunity and inflammation

Pom (44 decks)

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