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Year 1 POM > Immunity to infection: Sequence and timing > Flashcards

Immunity to infection: Sequence and timing Flashcards

1
Q

What are the steps of the immune response to infection?

A

Congenital immune deficiencies:

  1. Microbial Detection
  2. Innate immune response
    - Autoimmune and autoinflammatory diseases
  3. Adaptive immune response
  4. Memory response
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2
Q

What is part of the innate immune response?

A
  1. epithelia
  2. Phagocytes (neutrophils, macrophages, DC)
  3. NK cells
  4. . Innate lymphoid cells
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3
Q

What is part of adaptive immunity response?

A
  1. lymphoid tissues
  2. T and B lymphocytes
  3. Antibodies
  4. Cytoxic T cells response
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4
Q

What is part of memory response?

A
  1. T and B cells
  2. Quick and specific response
  3. Life long immunity
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5
Q

What are examples of extracellular pathogen niches during infection?

A

e.g. Staphylococcus, Streptococcus, Candida, microbiota, worms

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6
Q

What are examples of intracellular pathogen niches during infection?

A

e.g. Salmonella, Chlamydia, Legionella, Coxiella, Plasmodium, helminths

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7
Q

What are examples of surface adherent pathogen niches during infection?

A

e.g. enteropathogenic & enterohaemorrhagic E. coli

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8
Q

What are examples of intracellular by cytosolic pathogen niches during infection?

A

e.g. viruses, Listeria, Burkholderia, Mycobacterium

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9
Q

What are the characteristics of innate immunity?

A

Fast acting, first line of defence, germline encoded receptors

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10
Q

What are some physical barriers?

A

•Skin, mucous, epithelial cells

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11
Q

What is involved in the humoral response for innate immunity?

A

Complement, Lectins (collectins, ficolins), Pentraxins, Antimicrobial peptides

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12
Q

What cells are involved in infection for innate immunity?

A

•Neutrophils, Macrophages, Dendritic cells, Natural Killer (NK)-cells

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13
Q

What are the features in adaptive immunity?

A

Slower but long-lasting, variable receptors that mature over time (DNA recombination)

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14
Q

What is involved in the humoral response in adaptive immunity?

A
  • Antibodies (immunoglobulins of various types)

* Complement

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15
Q

What cells are involved in adaptive immunity ?

A

•Cytotoxic T-cells, T helper cells, T regulatory cells, B lymphocytes & Plasma cells

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16
Q

What are the differences in innate and adaptive immunity?

A
  • Timing of the response
  • Cell types
  • Receptors & ligands
  • Cytokines & chemokines
  • Molecular effector machineries
  • Both arms of the immune system together provide sterilising immunity and long-term memory
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17
Q

What is the specificity like in innate immunity?

A

For structures shared by called of microbes (pathogen-associated molecules patterns)

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18
Q

What is specificity like in a adaptive immunity?

A

for structural detail of microbial molecules (antigens); may recognise nonmicroblal antigens

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19
Q

What is the number of microbial molecule recognised in innate immunity?

A

About 1000 molecules patterns (estimated)

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20
Q

What is the number of microbial molecule recognised in adaptive immunity?

A

> 10^7 antigens

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21
Q

What are the receptor like in innate immunity?

A

Encoded in germiline; limited diversity (pattern recognition receptors)

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22
Q

What are the receptor like in adaptive immunity?

A

Encoded by genes produced by somatic recombination of gene segments; greater diversity

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23
Q

What is the number and types of receptors in innate immunity?

A

<100 different types of invariant receptors

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24
Q

What is the number and types of receptors in adaptive immunity?

A

Only 2 types of receptors (Ig and TCR) with millions of variations of each

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25
Q

What is the distribution of receptors in innate immunity?

A

Nonclonal: Identical receptors on all cells of the same lineage

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26
Q

What is the distribution of receptors in a adaptive immunity?

A

Clonal: clones of lymphocytes with distinct specificities express different receptors

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27
Q

How does an immune response to infection start?

A
  1. Tissue damage

2. Detection of pathogens

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28
Q

What are the first responder in an immune response?

A

-neutrophils and macrophages
1. Neutrophils are the first to respond (short-lived, ~6 h), followed by macrophages
2, “Naïve” cells become “activated” upon interaction with microbes
3. Phagocytes control infection and limit/repair tissue damage
4. Uncontrolled activities of phagocytes is not good
5 .Granulomas
6. Excessive inflammation & inappropriate adaptive immunity
7. Tissue damage

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29
Q

What is the communication within the system?

A
  1. Microbial ligands - detection
  2. Naiive host cell - gene expression changes
  3. Cytokines and chemokines - signal transduction
  4. “activated” host cells
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30
Q

What are activated macrophages?

A

•Macrophages are tissue resident or circulatory (from bone-marrow)
•Macrophage “activation” = expression of many new genes
•Induced by microbes & cytokines
•“Alternatively” activated macrophages are anti-inflammatory
Crosstalk between macrophages & lymphocytes during infection by intracellular pathogens

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31
Q

What does activated macrophages display enhance?

A
  1. Phagocytosis & Migration
  2. Cytokine/chemokine production
  3. Expression of cell surface molecules
  4. Antimicrobial activity
  5. Antigen presentation & T cell activation
32
Q

What is an immune response for Bacteria?

A 
Immune response                           
•Inflammatory cytokines 
•Antimicrobial genes
•Metabolic genes
•Immunomodulatory genes
No immune response:
-Resolution of inflammation
33
Q

What is the immune response for fungi?

A
  • Proinflammatory cytokines
  • Antimicrobial genes
  • Metabolic genes
  • Immunomodulatory genes
34
Q

What is the immune repose for virsus?

A
  • Interferon production
  • Proinflammatory cytokines
  • Antiviral genes
  • Immunomodulatory genes
35
Q

What are interferons?

A
  • Interferons are special cytokines

* They have direct antiviral activities

36
Q

What are some antiviral genes?

A
  • Nucleases
  • Inhibitors of virus entry & exit
  • Inhibitors of viral uncoating and replication
  • Inhibitors of protein translation
  • Immunomodulatory roles
  • Enhanced T-cell responses
  • Anti-inflammatory actions
  • Tissue repair
37
Q

What are some innate immune cells?

A 
Neutrophils
Macrophages
Dendritic cells
NK cells
Complement
38
Q

What are barriers for innate immunity?

A

epithelium, acid, commensals etc

39
Q

When does innate immunity happen?

A

Hours – day(s)

“Non-specific” BUT different routes/cells for different pathogens

40
Q

What are interleukins?

A
  • Activate cells (via genes, transcription factors)

- Inflammation

41
Q

What are interferons?

A
  • Anti-viral cytokines

- Produced when cells infected, prevent further infection

42
Q

What do chemokine do?

A

-Bring cells to infection areas

43
Q

What are phagocytes?

A

-Neutrophils + macrophages
1. Detect pathogens by pathogen components (lipids etc) or cell damage
2. Activated:
Inflammatory cytokines + chemokines
3. Phagocytose pathogens + destroy them
-Reactive oxygen species (ROSs

44
Q

What are NK cells?

A
  • Kill virus-infected cells
  • Activated by activating/inhibitory signals on cells
  • These signals will change when cells are infected
45
Q

What is complement?

A
  • Protein cascade
  • Activated by pathogens entering body
  • Opsonise, lyse + neutralise pathogens
46
Q

What are dendritic cells?

A
  • Link between innate -> adaptive immunity
  • Located throughout the body, e.g. skin
  • Samples area
47
Q

What happens when dendritic cells detect pathogens?

A
  • Activates -> presents pathogen antigens via MHC I, II

- Moves to lymph node to activate T, B cells

48
Q

When does adaptive immunity happen?

A 
-5-7 days after infection
Takes time for cells to proliferate
-T cells
-B cells
-Pathogen-specific
So, much more effective at clearing pathogen
49
Q

What do T cells do?

A
  1. Cytotoxic (CD8+) and Helper (CD4+) T cells
  2. Helper T cells “help” activate B cells; produce cytokines
  3. Cytotoxic T cells kill virus infected cells
50
Q

What do B cells do?

A
  1. B cells differentiate into plasma cells
  2. Plasma cells -> produce pathogen-specific antibodies
    - These cover, neutralise + kill pathogens
51
Q

Why is the death of infected cells a paradox?

A
  • Virus-infected cells are killed by the actions of cytotoxic T lymphocytes (CTLs) or Natural Killer (NK) cells
  • Cell death removes viral replicative niches
  • CTLs and NK cells directly kill infected cells (contact-dependent)
  • Host cells infected with intracellular bacterial pathogens also undergo forms of cell death (contact-independent)
52
Q

What are soluble effector mechanisms?

A
  • Complement mediated bacterial destruction
  • Lectin-binding to neutralise cell attachment or entry
  • Iron chelation (siderophores) to prevent replication
  • Antibiotic-like peptides
53
Q

What are cellular effector mechanisms?

A
  • Reactive Oxygen and Nitrogen radicals

* Acidification and digestion within phagosomes

54
Q

What is the summary of innate immunity to infection?

A
  • Phagocytes are the first responders
  • Phagocytes are “activated” for more effective killing of pathogens
  • Inflammatory cytokines drive inflammation and adaptive immunity and interferons promote antiviral responses
  • Gene expression changes are important in phagocyte activation
55
Q

What do a activtaed macrophages and DCs present?

A

ntigens in combination with MHC-I or MHC-II to T cells

56
Q

What do cytokines produced by antigen presenting cell produce?

A
  • Cytokines produced by antigen-presenting cells produce a suitable milieu for T-cell activation
  • E.g. IL-12 promotes T-cell replication
57
Q

What to T cells provide?

A
  • T cells provide cytokines that activate phagocytes
  • E.g. IFNg upregulates MHC-II expression for antigen presentation
  • Responses are specific to general class of pathogens
58
Q

How doe T cells help B cells produce antibodies?

A
  • Antigen presenting cell activation by infection and cytokines
  • DCs, macrophages
  • T cell activation by cognate MHC + foreign peptide recognition
  • B cell activation for antibody production against antigen
  • Antibody-mediated enhanced antimicrobial response
  • Phagocytosis (opsonisation)
  • Complement activation
59
Q

Whats a broad classification of T cell functions?

A
  1. Phagocyte activation: enhanced killing of pathogens and inflammation
  2. Direct killing of infected cells: removal of replicative niches
  3. B cell activation: antibody production and affinity maturation
  4. Innate lymphoid cell/ gamma delta T cells: a type of early responders (MHC independent actions)
60
Q

What is Th1?

A
  1. Defining cytokines: IFN-gamma
  2. Principle target cells: macrophages
  3. Major immune reactions: macrophage activation
  4. Host defence: intracellular pathogens
  5. Role in disease: autoimmunity; chronic inflammation
61
Q

What is Th2?

A
  1. Defining cytokines: IL-4, IL-5, IL-13
  2. Principle target cells: Eosinophils
  3. Major immune reactions: Eosinophil and may cell activation; alternative macrophage activation
  4. Host defence: Heminths
  5. Role in disease: Allergy
62
Q

What is Th17?

A
  1. Defining cytokines: IL-17. IL22
  2. Principle target cells: Neutrophils
  3. Major immune reactions: Neutrophil recruitment and activation
  4. Host defence: Extracellular bacteria and. fungi
  5. Role in disease: Autoimmunity and inflammation
63
Q

What is a summary of. adaptive immunity to infection?

A
  • T and B cells play special roles in adaptive immunity
  • Lymphocytes rely on appropriate antigen presentation and innate immune responses
  • Long-term responses rely on memory T and B cells which can be quickly activated and deployed upon subsequent exposure to the same pathogen
64
Q

Whats the sequence of immune response?

A
  • Sequential change from “resting/naive” to “activated” state
  • Driven by gene expression changes driven by specific combination of cytokines
  • Naïve to activated macropahge
  • Differentiation of ‘precursor’ cells into specific lineages of cells
  • T cells to Th1/Th2/Th17 or other types
65
Q

What happens if complement defect?

A

Varied complement genes dysfunction

66
Q

What happens in leukocyte adhesion?

A

Dysfunction in genes involved in migration and adhesion

67
Q

What happens in chronic granulomatous disease?

A

Loss of reaction oxygen species production

68
Q

What happens in Chediak-Higashi syndrome?

A

Compromised lysosomes

69
Q

What happens in cytokine genes and their receptors?

A

Loss of cell-to-cell communication

70
Q

What happens in SCID?

A

Severe reduction and function of T and B cells

71
Q

What happens in X linked agammaaglobulinaemia?

A

Decrease seri, OgG of all types

72
Q

What happens in HIV?

A

reduced CD4 helper cells

73
Q

What happens in irradiation and chemotherapy (cancer treatment)?

A

Loss of bone marrow precursors

74
Q

What happens in immunosuppression (graft rejection/chronic disease)

A

Depletion or impairment of lymphocytes

75
Q

What is a summary of immunity to infection?

A
  • First responders detect infection and try to control microbial growth
  • Secreted effectors such as chemokines & cytokines trigger inflammation & activate cells
  • Phagocytes (DCs & macrophages), as well as B cells, present antigens and activate T cells
  • T cells activate B cells and together contribute to humoral and cellular immunity to infection
  • Genetic and environmental factors can predispose individuals to infections

Year 1 POM (39 decks)

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