Immune Response Flashcards

1
Q

What is an Adaptive Immune response?

A

Specific and can produce immunological memory.

  • Innate immune may be faster but can not change on re-exposure to infectious agent ( complement, phagocytosis, natural killer cells )
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2
Q

What two phases usually occur during an immune response?

A

Antigen recognition involving clonal selection and clonal expansion

Antigen eradication in the effector phase the immune response in coordinated

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3
Q

How do different bacterial niches cause differing responses?

A

EXTRACELLULAR: pathogen multiplies outside of cells and dies if moved into a phagocytes – e.g. staphylococcus, streptococcus, Candida, microbiota, worms

  • Are accessible to antibodies and complement

INTRACELLULAR vacuolar: pathogen replicates inside cells – e.g. salmonella, chlamydia, legionella, Coxiella, plasmodium, helminths

§ Not accessible to antibodies and complement so immune cells need to recognise and tackle infected host cell to get to pathogen

SURFACE ADHERENT: enteropathogenic + enterohaemorrhagic E. Coli

INTRACELLULAR CYTOSOLIC: viruses, listeria, burkholderia, mycobacterium

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4
Q

Which cellular components are use in innate immunity? (4)

A

Neutrophils
Macrophages
Dendritic cells
Natural Killer cells

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5
Q

Which cellular components are used in adaptive immunity? (5)

A
Cytotoxic T cell
T helper cells
T regulatory
B lymphocytes
Plasma cells
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6
Q

What structure(s) is the Innate system specific for?

How many molecules can be recognised?

A

Pathogen associated molecular patterns

PAMPs

1000 molecular patterns

e.g. Toll receptors on microbes identical

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7
Q

What structure(s) is the Adaptive system specific for?

How many molecules can be recognised?

A

Antigens

under 10^7

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8
Q

What allows the adaptive immune system to have a greater diversity of receptors compared to innate?

A

Innate receptors are encoded in germline ( <100 )

Adaptive receptors are encoded by somatic recombination of gene segments ( Ig and TCR with millions of variation )

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9
Q

How does the innate and adaptive immune system communicate?

A

Soluble messengers e.g. interleukins and interferons

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10
Q

How are phagocyte responses pathogen specific?

A

Specificity starts w/pathogen-specific responses made by macrophages – leads to activation of those phagocytes turning on specific gene expression programmes + inducing secretion of various interleukins and soluble mediators

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11
Q

Which genes are utilised in phagocyte responses?

A

Antimicrobial genes
Metabolic genes
Immunomodulatory genes

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12
Q

What is it about bacterial that triggers phagocytosis?

A

Alive bacteria phagocytosed released mRNA

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13
Q

How do interferons promote antiviral defence?

A

Release of interferons promotes antiviral defence

Interferons are special cytokines with direct antiviral activities

Antiviral genes include: NucleasesInhibitors of virus entry & exit
Inhibitors of viral uncoating and replication
Inhibitors of protein translation

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14
Q

How do phagocytosed microbes be killed - involves macrophages?

A

Macrophages are tissue resident or circulatory (from bone-marrow)

  • Macrophage “activation” = expression of many new genes
  • Induced by microbes & cytokines
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15
Q

What is enhanced when macrophages are activated? 5

A

phagocytosis and migration

cytokine/chemokine production

expression of cell surface molecules

antimicrobial activity

antigen presentation and T cell activation

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16
Q

What immunomodulatory roles do interferons play?

A

Enhanced T cell responses

anti Inflammatory

tissue repair

17
Q

How are virus infected cells killed?

A

CTLs
NKs

They kill infected cells by directly contacting them ( contact-dependent )

  • contact independent cell death would be for intracellular bacterial pathogens
18
Q

What are the 4 examples of soluable effector mechanisms ( Humoral )

A

Complement bacterial destruction

Lectin binding to neutralise cell

Iron chelation to stop replication

Antibiotic like peptides

19
Q

What are are some examples of cellular effector mechanisms?

A

Reactive Oxygen and Nitrogen radicals

Acidification and digestion within phagosomes.

  • Microbes are killed by: phagocyte oxidase, Nitric oxide, phagocytosis
  • Inflammatory enhancement by : Cytokines activated by humoral immunity.
  • Understand connection between Humoral affects linked to cellular affects
20
Q

Which Interferons promote antiviral responses?

A

Type I and II

21
Q

Which Interferon promotes antibacterial immunity?

A

Type II

22
Q

How do activated macrophages and DCs present antigens to T cells?

A

MHC-1

MHC 2

23
Q

How the APCs activate T cell replication?

A

Cytokines produced for example IL-12 from APCs trigger T cells

  • APCs are macrophages and DCs
24
Q

How can activated macrophages and DCs lead to activated phagocytes?

A

T cells activated produce cytokines to activate the phagocytes.

e.g. IFN-gamma enhances macrophage expression of more genes and can increase APC presentation

25
Q

How do T cells help B cells produce antibodies?

A

T cells interact with APCs and become activated themselves by recognising the foreign peptides

Then Help B cell to become activated by putting peptide on BCR

B cell produce antibody against antigen present on BCR

26
Q

Which T cells work against viruses and bacteria respectively?

A

Th1 Cell = CD4 T cell

Cytotoxic T cell = CD8 T cell

27
Q

How can T cells work independently of MHCs?

A

Innate lymphoid cells = Gammadelta T cells

28
Q

Effector T cell : Th1

Cytokine?
Target cell?
Immune effect?
What pathogen?
Role in disease?
A

Cytokine = IFN- Gamma

Target cell = Macrophages

Immune effect = Macrophage activation

What pathogen = Intracellular pathogens

Role in disease = Autoimmunity. chronic inflammation if uncontrolled

29
Q

Effector T Cell : Th2

Cytokine?
Target cell?
Immune effect?
What pathogen?
Role in disease?
A

Cytokines = IL-4 , IL-5, IL-13

Target cell = Eosinophil

Immune effect = Eosinophil activation

What pathogen = Helminths

Role in disease = Allergy

30
Q

Effector T Cel : Th17

Cytokine?
Target cell?
Immune effect?
What pathogen?
Role in disease?
A

Cytokine = IL-17, IL-22

Target cell = Neutrophils

Immune effect = Neutrophil recruitment and activation

What pathogen = Extracellular bacterial and fungi

Role in disease = Autoimmune inflammation

31
Q

What drives the change from naive to activated immunity?

A

Gene expression changes through cytokine combinations.

Differentiation of precursor cells into specific cells e.g. T cells to Th1 Th2 Th17 etc

32
Q

In the first 12 hours after infection, what occurs?

A
Innate immunity:
Phagocytes
Mast cells
Epithelial barrier
DCs
NKs
ILCs
Complement
33
Q

What occurs in the days following infection?

A

Adaptive immunity:
B lymphocytes recognise antigen –> proliferate –> differentiate into plasma or memory
T Lymphocytes recognise antigen –> Proliferate –> differentiate into Memory or effector

34
Q

What is the impact of age on the immune response?

A

As age increases:

Naive T cells in blood decreases

Memory T cells in blood increase

Thymic output decreases