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Phase 2 > Immunology > Flashcards

Immunology Flashcards

1
Q

What is innate immunity?

A

Non-specific immune response to pathogens

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2
Q

What is adaptive immunity?

A

Specific acquired ammunity

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3
Q

What cells are polymorphonuclear leukocytes?

A
  • Neutrophil
  • Eosinophil
  • Basophil
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4
Q

What cells are mononuclear leukocytes?

A
  • Monocytes
  • T cells
  • B cells
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5
Q

What are the cells of the immune system?

A
  • Neutrophils (65%)
  • Eosinophil (5%)
  • Basophil (0.2%)
  • Monocytes (5%)
  • T cells (10%)
  • B cells (15%)
  • Mast cells
  • Natural killer cells (15%)
  • Dendritic cells
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6
Q

What are the two main types of intracellular granules that neutrophils have?

A
  1. Primary - myeloperioxidase, muramidase, acid hydrolases, proteins
  2. Secondary - lactoferrin, lysosome
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7
Q

What receptors do monocytes have on their cell wall?

A
  • Fc
  • Complement
  • PRR
  • Toll-like
  • Mannose
  • Scavenger
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8
Q

What receptor is expressed on eosinophils?

A

CD125 receptor

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9
Q

What is in eosin granules?

A

Major Basic Protein - this is toxic to helminth worms and activates neutrophils and induces histamine release from mast cells and promotes bronchospasms.

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10
Q

What are mast cells?

A
  • Tissue cells which are similar to basophils

- Express IgE receptor, binding to this receptor causes degranulation of histamine

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11
Q

What are the four types of T cell and their role?

A
  1. T helper 1 – CD4 help immune response to intracellular pathogens
  2. T helper 2 – CD4 help produce antibodies to extracellular pathogens
  3. Cytotoxic T cell – CD8 can kill directly
  4. T regulatory (FoxP3 receptor) – regulate immune response and dampen the response
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12
Q

What receptors do B cells have?

A

CD19 and CD20

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13
Q

What cells do B cells mature into?

A

Plasma cells - these produce antibodies

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14
Q

What is the role of natural killer cells?

A

To recognise and kill virus infected cells and tumour cells

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15
Q

What are the three actions of the compliment pathway?

A
  1. Direct lysis
  2. Attract more leukocytes to the site of infection (chemotaxis)
  3. Coat invading organisms with C3b (opsonisation)
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16
Q

What are the 5 different types of antibodies?

A
  1. IgG
  2. IgA
  3. IgM
  4. IgD
  5. IgE
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17
Q

Definition of antibody

A

Protein produced in response to an antigen. It can only bind with the antigen that induced its formation.

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18
Q

Definition of antigen

A

Molecule that reacts with preformed antibodies and specific receptors on T and B cells

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19
Q

Definition of epitope

A

Part of an antigen that binds to the antibody/receptor binding site

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20
Q

Definition of affinity

A

Measure of the binding strength between the epitope and an antibody binding site.

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21
Q

What are cytokines and four examples of cytokines:

A

Signalling proteins secreted by immune and non-immune cells

  • Interferons
  • Interleukins
  • Colony stimulating factors
  • Tumour necrosis factor
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22
Q

What are chemokines?

A

Group of 40 proteins which direct movement of leukocytes and other cells from the blood stream to tissue or lymph organs

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23
Q

What components make up the innate immune system?

A 
Anatomical barriers
Mucous membranes
Physiological barriers
Phagocytic cells
Serum proteins (complement)
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24
Q

What is the inflammatory process following tissue damage?

A
  1. Stop the bleeding – coagulation
  2. Acute inflammation – leukocyte recruitment
  3. Kill pathogens, neutralise toxins, limit pathogen spread
  4. Clear pathogens – phagocytosis
  5. Proliferation of cells to repair damage
  6. Remove blood clot and remodel the extracellular matrix
  7. Re-establish normal structure and function of tissue
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25
Q

What are the two killing pathways present in neutrophils and macrophages?

A
  1. O2 independent - lysosomes, defensins, TNF, pH

2. O2 dependent - free radicals

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26
Q

What is neutrophil extravasion following bacterial infection?

A

Movement of neutrophils from blood vessels into surrounding tissue in response to chemokine secretion from tissue macrophages

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27
Q

Explain the process of phagocytosis:

A
  1. Pathogen is recognised by cell surface receptors on macrophage
  2. Macrophage endocytoses the pathogen into a phagosome
  3. The phagosome fuses with a lysosome to form a phagolysosome
  4. Pathogen is degraded in the phagolysosome
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28
Q

What is passive immunisation

A

The transfer of preformed antibodies between humans

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29
Q

Two examples of passive immunisation

A

Transfer of maternal antibodies across the placenta

Transfer of maternal antibodies through breast milk

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30
Q

One example of unnatural immunisation

A

Treatment of immunocompromised patients with immunoserum

31
Q

What is a disadvantage of passive immunisation?

A

It does not elicit immunological memory, merely neutralises toxins with the finite amount of anti-toxins

32
Q

Where can passive immunisation be used clinically?

A

To treat snake bites, jelly fish stings

As a prophylaxis to prevent an infection following exposure to hepatitis/measles/rabies

33
Q

What is active immunisation?

A

Manipulation of the immune system to generate a persistent protective response against pathogens by safely mimicking natural infection.

34
Q

What is the predominant immunoglobulin in primary exposure to a pathogen?

A

IgM - low-affinity non-specific

35
Q

What is the predominant immunoglobulin in secondary exposure to a pathogen?

A

IgG - high-affinity highly-specific

36
Q

What are the 5 types of vaccine design?

A
  1. Whole organism - live attenuated or killed inactivated
  2. Subunit
  3. Synthetic peptide
  4. DNA vaccines
  5. Engineered virus - recombinant vector vaccines
37
Q

What is a vaccine adjuvant?

A

Substances added to a vaccine to stimulate the immune system

38
Q

Why do we need the adaptive immune system?

A
  • Some microbes can evade the innate immune system
  • Intracellular viruses and bacteria hide in cells
  • Immunological memory
39
Q

What cells are involved in the immune system?

A

T cells and B cells

40
Q

Where do T cells mature?

A

Thymus

41
Q

Where do B cells mature

A

Bone marrow

42
Q

What other molecules are required for the adaptive immune system to function?

A
  • Major histocompatibility complex
  • Intrinsic/endogenous/intracellular antigens
  • Extrinsic/exogenous/extracellular antigens
43
Q

What type of antigens do T cells respond to?

A

Intracellular presented antigens (not soluble antigens)

44
Q

What is T cell selection?

A

The process of T cells which recognise self-tissue being killed in the foetal thymus to prevent autoimmunity

45
Q

What other immune structure is a T cell receptor similar to?

A

Fab region of an antibody

46
Q

How are intracellular viruses processed by nucleated cells and presented to T cells?

A

Viral proteins are broken down and presented on the cell surface alongside MCH1. These are recognised by CD8 T cells and destroyed.

47
Q

How are CD8 cells activated?

A

WHen they react with MHC1/peptide the CD8 cells is activated into a cytotoxic T cell. This produces proteolytic granules and released perforins and granulysin which damage the infected cell.

48
Q

How are CD4 cells activated

A

APC presents the antigen via MHC2. Interleuekin 12 produced by APC causes activation of CD4 cell into Th1 cell.
Production of interleukin 2 by the T cell stimulates activation into Th2 cell ???

49
Q

What is clonal expansion?

A

Replication and proliferation of Th2 cells

50
Q

What is humoral adaptive immunity?

A

Antibody mediated immunity

51
Q

Are B cells antigen presenting cells?

A

Yes

52
Q

What is the process of gaining humoral immunity?

A
  • Antigen interacts with B cell receptor
  • B cell ingulf antigen and process antigen
  • B cell presents antigen alongside MHC2
  • T cell receptor (Th2) binds to B cell and secrete IL4,5,10,13
  • B cells either differentiate into plasma cells or memory cells
  • Plasma cells produce more antibodies
  • Memory cells remain in the circulation and are activated into plasma cells
53
Q

What is the neutropaenic phase in cancer patients following chemotherapy?

A

The 2-4 week phase were patients don’t have any circulating neutrophils

54
Q

What is a pattern recognition receptor?

A

A molecule that recognises patterns on harmful foreign bodies that stimulates an immune response despite no previous exposure.

55
Q

What components/features of gram -ve cell walls make them identifiable by PRRs?

A
  • Lipopolysaccharides
  • Peptidoglycans
  • Hydrophobicity
56
Q

What components/features of gram +ve cell walls make them identifiable by PRRs?

A
  • Acidic polysaccharides

- Peptidoglycans

57
Q

What are the secreted and circulating PRRs?

A 
Antimicrobial peptides (secreted in lining fluids) - defensins, cathelicidin 
Lectins and collectins e.g. mannose binding lectin, work by binding to carbohydrates/lipids in microbe walls and activating complement and phagocytosis
Pentraxins e.g. C-Reactive Protein which have antimicrobial actions (interact with C protein of pneumococci and activate complement)
58
Q

What are the cell associated PRRs?

A
  • Toll-like receptor
  • Mannose binding receptor on macrophages (recognise fungi)
  • Dectin-1 found on phagocytes (recognise beta glucans in fungi)
  • Scavenger receptor on macrophages
  • Nod-like receptor
  • Rig-like receptor
59
Q

What does TLR1/2 recognise?

A

Gram +ve bacteria lipopeptides

60
Q

What does TLR3 recognise?

A

Double stranded viral RNA

61
Q

What does TLR4 recognise?

A

Lipopolysaccharides on gram -ve bacteria, viral proteins, pneumolysin

62
Q

What does TLR5 recognise?

A

Flagellin (bacterial motor protein)

63
Q

What does TLR2/6 recognise?

A

Gram +ve lipopeptides

64
Q

What does TLR7 recognise?

A

Single stranded RNA

65
Q

What does TLR8 recognise?

A

Single stranded RNA

66
Q

What does TLR9 recognise?

A

Bacterial DNA as there is an extra methyl group on cytosine residues of bacterial DNA

67
Q

What do TLRs do?

A

Activate pro-inflammatory gene transcription and promote antiviral immunity through enhancing NF-kappaB driven inflammation and stimulating interferon release

68
Q

How do nod-like receptors detect intracellular pathogens?

A

Detect peptidoglycans and muramyl dipeptide.

NOD2 - recognises muramyl dipeptide which is a breakdown product of peptidoglycan in gram +ve cell walls

69
Q

What disease arises from over-active NOD2 receptor?

A

Blau’s syndrome - chronic granulomatous inflammation of the skin and eyes

70
Q

What disease arises from under-active NOD2 receptor?

A

Chron’s disease

71
Q

What are Rig-like helicase receptors?

A

Receptors which detect double stranded viral RNA and DNA.

They stimulate interferon production facilitating an antiviral response

72
Q

Why does the innate immune system also deal with tissue damage?

A

Innate immune system is also triggered by damage molecules released from the body.

73
Q

What are cellular damage molecules?

A
  • Fibrinogen
  • Hyaluronic acid
  • Tenascin C
  • HMGB1
  • mRNA
  • Heat shock proteins
  • Uric acid
  • Stathmin
74
Q

Where can TLR receptor agonists be used clinically?

A
  • Vaccine adjuvants to stimulate an immune response

- Skin cancer ointments to elicit an immune response against the cancerous cells

Phase 2 (6 decks)

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