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FBS 2 > Immunity and Infection > Flashcards

Immunity and Infection Flashcards

1
Q

What are cluster of differentiation markers?

A

They are cell-surface markers that are used to delineate leukocyte populations.

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2
Q

What are the primary lymphoid organs?

A
  • Thymus

- Bone marrow

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3
Q

What are the secondary lymphoid organs?

A
  • Nasopharangeal lymph nodes
  • Tonsils
  • Bronchial lymph nodes
  • Peripheral lymph nodes
  • Spleen
  • Gut-associated lymphoid tissue (Peyer’s patches and appendix)
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4
Q

What are the six types of molecule that make up the immune system?

A
  • Defensins
  • Complement
  • Chemokines
  • Cytokines
  • Antibodies
  • T-cell receptors
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5
Q

What molecules are found in the adaptive and innate immune systems?

A

Innate = defensins, complement, chemokines, cytokines.

Adaptive = chemokines, cytokines, antibodes and T-cell receptors.

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6
Q

What are defensins?

A

They are anti-microbial peptides that disrupt microbial cell membranes and act as sensors microbe structures. They are secreted by epithelial and immune cells.

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7
Q

What are the roles of chemokines?

A
  • Attract cells along a gradient.
  • Recruit cells to sites of inflammation.
  • Responsible for separation of lymphocytes in tissues into zones.
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8
Q

What is a nosocomial infection?

A

When the disease arises in a hospital.

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9
Q

What is the innate immune response?

A

A non-specific defence mechanism that a host uses immediately or within several hours (0-96) after exposure to the antigen.

You are born with this response.

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10
Q

Apart from being a physical barrier, how does the skin help the innate immune response?

A

It produces anti-bacterial compounds.

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11
Q

What is PAMP?

A

The innate immune response’s way of recognising a few highly conserved molecular structures present in many different microorganisms.

P = pathogen
A = associated
M = molecular 
P = patterns
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12
Q

What are the two conditions that PAMP must fill?

A

1) Must be present in the microorganism but not the host.

2) Must be essential for the survival of the pathogen.

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13
Q

What is an example of a PAMP?

A

Lipopolysaccharaide (LPS) which is present in the cell walls of all gram negative bacteria and lipoteichoic acid which is present in the cell walls of all gram positive bacteria.

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14
Q

What are PRR?

A

Pattern Recognition Receptors recognise PAMPs and when bound, signal to the host cell nucleus triggering an upregulation of molecules associated with the immune response.

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15
Q

What are the three types of PRR?

A

1) Collectins (float in serum).
2) Toll-like receptors (membrane bound).
3) Nod-like receptors (found in the cytoplasm).

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16
Q

What are the two parts of collectin molecules and what are their functions?

A

1) Collagen-like region interacts with the effector parts of the immune system.
2) Lectin region binds to sugar molecules of the surface of pathogens (specifically manose).

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17
Q

How do collectins differ between manose in the host and manose in the pathogen?

A

By the molecular spacing.

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18
Q

How do Toll-like receptors work?

A

There are 10 different types that recognise a variety of different pathogenic components.

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19
Q

What is complement?

A

A series of proteins that circulate in the blood and tissue fluids that operate via a cascade.

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20
Q

What is the key protein in complement?

A

C3 which is activated by C3 convertase.

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21
Q

What are the three complement pathways and what are they activated by?

A

1) Classical = activated by an antigen-antibody complex.
2) MB-lectin = activated by mannose on pathogen.
3) Alternative = spontaneous activation by pathogen.

All of these pathways lead to the activation of C3 convertase.

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22
Q

What triggers recruitment phagocytosis?

A

C4a, C3a and C5a molecules.

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23
Q

What is opsonisation and what is it triggered by?

A

Where pathogens are targeted for distruction by phagocytes.

Triggered by C3b molecule.

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24
Q

What forms the membrane attack complex (MAC) and what does this do?

A

C5b, C6, 7, 8, 9

Form a pore that inserts into bacterial cell walls disrupting the osmotic gradient causing the bacteria to undergo lysis (explode).

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25
Q

What are the two cells in the innate immune response that undergo phagocytosis and antimicrobial killing?

A

Macrophages in tissues, monocytes in blood.

Neutrophils.

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26
Q

What are the features of macrophages?

A
  • Found in large numbers in the GI tract, liver and spleen.

- Relatively long-lived.

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27
Q

What are the features of neutrophils?

A
  • Found only in blood and travel to tissues only when needed.
  • Short-lived.
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28
Q

What does pus consist of?

A

Dead neutrophils with its dead bacterial cargo.

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29
Q

What is phagocytosis?

A

Recognition of the pathogen by receptors on the phagocyte leading to the ingestion and destruction of the pathogen.

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30
Q

What are the seven stages of phagocytosis?

A

1) Chemotaxis and adherence of microbe to phagocyte.
2) Ingestion of microbe by phagocyte.
3) Formation of phagosome.
4) Fusion of the phagosome with a lysosome to form a phagolysosome.
5) Digestion of ingested microbe by enzymes found in lysosome.
6) Formation of residual body containing indigestible material.
7) Discharge of waste materials by exocytosis.

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31
Q

What happens in phagocytosis that helps the later part of the immune response?

A

Proteins and peptides produced in the phagocytosis process are not exocytosed, but are displayed on the cell surface instead in order to convey a signal.

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32
Q

What is the respiratory burst?

A

A rapid increase in the intake of O2 following phagocytosis which leads to the production of oxygen radicals by NADPH oxidase. These oxygen radicals then go on to do DNA damage and alter bacterial membranes.

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33
Q

What does the cell do in order to prevent itself being damaged by the oxygen radicals produced in the respiratory burst?

A

1) They are rapidly converted into water and oxygen.

2) The assembly of the NADPH oxidase is in very close proximity to the pathogen.

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34
Q

How are reactive nitrogen intermediates produced?

A

When L-arginine goes to L-citrulline catalysed by nitric oxide synthase.

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35
Q

How is NO synthase activated?

A

By interferon gamma and tumor necrosis factor binding to their receptors on the phagocyte surface.

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36
Q

What are cytokines?

A

Small proteins that act as intercellular messengers that bind to specific receptors and have either an activating or deactivating response.

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37
Q

What is the role of cytokines in the innate immune response? Give examples.

A

They are mainly activating.

  • IL-1 (interleukin)
  • IL-6
  • TNFα (tumour necrosis factor)
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38
Q

What are chemokines?

A

They are a class of cytokines with chemoattractant properties which recruits cells to sites of inflammation.

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39
Q

How do chemokines promote inflammation?

A

By enabling cells to adhere to the surface of blood vessels and migrate to infected tissues.

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40
Q

When are type 1 interferons produced?

A

In the innate immune response in response to virally infected cells.

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41
Q

What are natural killer cells?

A

Triggered by type 1 interferons, they are cells capable of killing virally infected cells and tumour cells and are a source of interferon gamma.

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42
Q

What is IL-8?

A

Chemokine produced by macrophages and endothelial cells that recruits neutrophils to the site of infection.

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43
Q

What two things do naive t-cells require in order for them to become effector T-cells?

A

1) Recognition of the MHC signal on the surface of the antigen presenting cell which is produced during phagocytosis of the pathogen strongly enough to cause sustained signalling in the t-cell = signal one.
2) Recognition of CD86 signal which is caused by PAMP recognising a pathogen = co-stimulation or signal two.

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44
Q

What can be antigen presenting cells?

A

Macrophages
B-cells
Dendritic cells (best)

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45
Q

What happens when dendritic cells become mature?

A

Lots of dendrites covered in many signals associated with T-cell activation (MHC and CD86 molecules).

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46
Q

What do MHC and CD86 bind to on the T-cells?

A

MHC -> TCR

CD86 -> CD28

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47
Q

What are T-cell receptors composed of?

A

Two chains forming a membrane bound heterodimer. They consist of variable and constant domains.

They form a unique antigen binding site.

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48
Q

What are T and B cells actually called?

A

T and B lymphocytes.

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49
Q

What increases the probability that lymphocytes will encounter their specific antigen?

A

They constantly migrate through blood and lymphoid tissues.

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50
Q

What happens when lymphocytes encounter and bind to a specific antigen?

A

Binding causes them to divide rapidly. When the pathogens have been overcome, the increased number of cells remain but they enter a quiescent state.

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51
Q

How long can it take for the adaptive immune response to generate a primary and secondary response?

A

Primary = 12 days

Secondary = 5-7 days

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52
Q

What are the two regions of T and B cell receptors?

A

Variable = where the antigen binding diversity arises.

Constant

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53
Q

What are the three parts of the variable region of an antibody heavy chain?

A

1) Variable
2) Diversity
3) Joining

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54
Q

How many different combinations can be use in the antibody heavy chain variable region?

A

48V x 27D x 6J = 7776

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55
Q

What is the difference in segments between light and heavy antibody chains?

A

The light chain does not have a diversity segment.

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56
Q

What is combinatorial diversity?

A

The combination of segments together to generate unique receptors from multiple alternative segments in the germline genes.

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57
Q

How does junctional diversity introduce further diversity to antibodies?

A

When the different segments are joined together in the heavy and light chains, nucleotides are added and removed from junctions during rearrangement and this is not precise so some nucleotides may be lose or added which contributes to diversity.

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58
Q

What is gene rearrangement?

A

The random selection of V, D and J segments from the genome to form heavy and light chains of antibodies.

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59
Q

Where does gene rearrangement occur for B and T cells?

A

B = bone marrow

T = thymus gland

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60
Q

What are the two types of T-cell?

A

Cytotoxic

Helper

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61
Q

What happens when cytotoxic T-cells bind to an antigen?

A

They differentiate to secrete cytotoxic granules.

Binding to an antigen is all that the cells need to cause a response.

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62
Q

What happens when B-cells bind to an antigen?

A

They differentiate to form an antibody producing plasma cell producing antibodies with the same specificity as the B-cell receptor.

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63
Q

What happens when a helper T-cell binds to an antigen?

A

It differentiates to cells that are capable of producing a range of different cytokines (one cytokine is specific to one cell, but it can differentiate into many different types of cells).

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64
Q

What is another name for antibody?

A

Immunoglobulin. The two can be used interchangeably.

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65
Q

What are the two forms that antibody light chains can take?

A

Kappa or lambda - antibodies are never both just one or the other.

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66
Q

What binds heavy and light chains together in antibodies??

A

Disulphide bonds

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67
Q

What does the constant region of an antibody determine?

A

Its function.

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68
Q

What are IgM, IgG and IgA?

A

Different classes or isotopes of antibody defined by the constant regions of the heavy chains.

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69
Q

What are IgG1, IgG2 and IgA1 etc?

A

They are the subclasses of antibodies that are coded for by different constant region gene segments.

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70
Q

What is the Fc?

A

The paired constant region segments. Macrophages have many Fc receptors.

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71
Q

What are the general functions of antibodies?

A
  • Neutralise toxins and viruses by binding to them and stopping their interactions.
  • Opsonise pathogens by binding to them promoting phagocytosis by recognition of Fc receptors.
  • Activate the complement cascade.
  • Agglutinates particles (clumps them together).
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72
Q

What is the main serum antibody?

A

IgG

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73
Q

What is IgG good at?

A

Opsonisation. They coat pathogens so phagocytes and natural killer cells can recognise them.

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74
Q

What is antibody-dependent cellular cytotoxicity?

A

When pathogens are coated in IgG so become targets for natural killer cells.

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75
Q

How many subclasses of IgG are there and what are they named after?

A

4 subclasses that are named by increasing concentration in serum (1 is most abundant and 4 is the least).

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76
Q

How are IgA dimers formed?

A

By the joining of the constant end by a J chain.

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77
Q

Where to IgA dimers have a specific function?

A

On mucosal surfaces

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78
Q

How does IgA regulate the gut bacteria population?

A

IgA dimers produced by antibody producing plasma cells in the blood bind to receptors called secretory component on the basolateral surface of the epithelial cells in the gut. This allows IgA dimers to be transported into the lumen of the gut through the epithelia. IgA can then then 1) agglutinate and neutralise the bacteria found in the gut because they have four binding sites or 2) the secretory component receptor binds to mucus which adheres IgA and any bacteria bound to it to the epithelial walls of the gut lumen preventing their function.

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79
Q

What is the first antibody used in the immune response?

A

IgM

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80
Q

What does it mean if an antibody has high avidity?

A

It has a number of binding sites e.g. panteric IgM.

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81
Q

What does IgE work with?

A

Mast cells.

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82
Q

What happens when an allergen such as pollen interacts with IgE bound to mast cells?

A

This triggers degranulation of mast cells which gives the patient the symptoms of that allergy (sneezing, runny nose etc).

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83
Q

What are IgM and IgD found together?

A

Expressed on the surface of newly formed B cells with the same specificity.

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84
Q

What does secondary lymphoid tissue contain?

A

Zones of dividing B cells called germinal centres. B cells enter these centres after an encounter with a specific antigen and help from T cells.

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85
Q

What happens to B cells when they are in the germinal centre?

A

They divide and start to mutate their antibody/immunoglobulin variable region genes in heavy and light chains by somatic hypermutation which produces slightly different antigen specificities.

A range of different B cells are produced and are tested to see which one binds best to the antigen. The one that does goes on to proliferate.

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86
Q

What is affinity maturation?

A

The combination of somatic hypermutation and selection that occurs to B cells when they are in the germinal centres of lymphoid tissue.

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87
Q

Aside from affinity maturation, what else can B cells due in the germinal centres?

A

Class switch i.e. they change their constant regions of antibodies and go from IgM and IgD to other Igs such a IgA.

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88
Q

What are the two populations of B cells that leave the germinal centre?

A

1) Memory cells that are quiescent, have undergone affinity maturation and possibly class switching.
2) Plasma cells that localise in bone marrow (produce IgG) or the gut (produce IgA). These are the cells that can secrete protective antibodies for a lifetime.

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89
Q

What are monoclonal antibodies?

A

Powerful laboratory reagents and biological therapeutics used to treat a range of diseases including autoimmune, inflammatory and cancer - they are a population of identical antibodies.

These are created when a single B cell with a single desired specificity is expanded as a clone.

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90
Q

What does a polyclonal response mean?

A

Where a range of B cells and their antibodies with different specificities work together to recognise different components of the antigen.

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91
Q

Why do mouse monoclonal antibodies not make good therapeutics?

A

The mouse protein is seen as a foreign antigen so an immune response against the antigen is generated.

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92
Q

What is a chimeric antibody?

A

The variable region of the antibody is from a mouse and the constant region is human.

Chimeric antibodies have the ending -ximab.

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93
Q

What is an example for use of monoclonal antibodies?

A

Rituximab is an antibody to CD20. CD20 is expressed by B cells so Rituximab can target B cells for killing in B cell lymphomas and rheumatoid arthritis.

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94
Q

What is humanisation of monoclonal antibodies?

A

Where the variable region is modified even further so that the only part that is from the mouse are the sections that bind to the antigen.

These have the ending -zumab.

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95
Q

What ending do entirely human monoclonal antibodies have?

A

-umab

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96
Q

How does a person inherit A, B and AB blood types?

A

A = both parents have A or one with O and one with A.

B = both parents have B or one with O and one with B.

AB = one parent has B and one parent has A.

This is an example of co-dominance.

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97
Q

What does someone with O and AB blood types mean for their circulating antibodies?

A

O = they have circulating antibodies that recognises both A and B antigens. This means that they do not react with any blood type antibodies making them the universal donor.

AB = they have no circulating antibodies for blood type antigens. This makes them the universal acceptors of blood types.

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98
Q

What happens when a rhesus negative woman is pregnant with a rhesus positive baby and then has another pregnancy?

A

When her blood is exposed to the baby’s blood with the Rh+ antigens, her immune system produces antibodies that recognise this. This is not a problem in the first pregnancy, but if a second pregnancy is Rh+, the anti-Rh+ IgG antibodies are able to cross the placenta so cause red blood cell lysis in the foetus and haemolytic disease of the newborn.

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99
Q

How is haemolytic disease of the newborn treated?

A

Plasmapheresis to remove the harmful anti-Rh+ IgG antibodies.

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2
3
4
5
Perfectly
100
Q

What immune cell type is lost in an HIV infection?

A

CD4 T-cells

101
Q

What do t-cell receptors recognise?

A

Foreign molecules (e.g. peptide antigens) that are bound to a self-protein coded for by MHC (major histocompatibility complex) genes found on antigen-presenting cells.

102
Q

What are the features of MHCI proteins?

A
  • Associates with β2 microglobulin.
  • Endogenously expressed on all nucleated cells.
  • Has a peptide-binding groove at the distal end.
103
Q

What are the features of MHCII proteins?

A
  • αβ heterodimer.
  • Expressed on specialised antigen-presenting cells including monocytes, macrophages, dendritic cells and B lymphocytes.
  • Has a peptide-binding groove at the distal end.
104
Q

What peptides do MHCI molecules expressed?

A

Peptides derived from proteins that are currently being synthesised in the cell.

This includes viruses.

105
Q

What peptides do MHCII molecules express?

A

Peptides derived from antigens that they have ingested from outside.

106
Q

How does MHCI help the immune system recognise a viral infection?

A

Viruses invade the cell and hijacks the cell’s protein production machinery in order for it to replicate.

Because MHCI presents peptides derived from ALL proteins produced by the cell, part of the invading virus is also presented.

107
Q

How do antigen-presenting cells express antigen peptides on MHCII molecules?

A

When an antigen is taken into the cell, it is enveloped by a vesicle that contain proteolytic enzymes that degrade the antigen. At the same time, MHCII is being synthesised and assembled in the endoplasmic reticulum. They then fuse with the vesicles containing the degraded antigen, load their peptide and then travel to the cell surface.

108
Q

Where are the genes coding for MHCI & II found?

A

On the short arm of chromosome 6.

These genes are polymorphic and polygenic and are codominantly expressed.

109
Q

Where is the polymorphism of MHC molecules found?

A

In the peptide binding groove.

110
Q

What are the two subtypes of T-cell receptors?

A

1) αβ

2) γδ

111
Q

How are T-cell receptor heterodimers arranged?

A

In a similar way to antibodies - they have V, D, J and C regions (alpha chain has no D region) that have many different gene variations and rearrangements making millions of different receptors.

112
Q

Which part of the T-cell receptor has the most variation?

A

The part that interacts with the MHC molecule.

113
Q

What type of T-cells interact with MHCI molecules?

A

CD8 t-cells (cytotoxic cells). These cells kill cells infected with viruses.

CD8 interacts with the constant part of the MHCI molecule.

114
Q

What type of T-cells interact with MHCII molecules?

A

CD4 t-cells (helper cells)

CD4 interacts with the constant part of the MHCII molecule.

115
Q

What happens when T-cells become activated?

A

They begin to divide and produce cytokines.

116
Q

What happens when helper T-cells become activated?

A

They differentiate into different kinds of EFFECTOR t-cells with different distinct functions.

117
Q

What are CD4+ Treg and what is their function?

A

They are regulatory helper T-cells that have differentiated in response to being activated.

Their role is to prevent immunopathology by modulating the activity of other immune cells.

118
Q

What are the functions of the T-helper cell Th1?

A

They secrete IFN-γ (aids differentiation and activation of macrophages) and IL-2 (aids CD8 t-cells and helps them to proliferate and secrete cytokines) and are mainly involved in viral infections and other intracellular pathogens.

119
Q

What are the functions of the T-helper cell Th2?

A

They are mainly involved in extracellular parasites. They produce IL-4 and -13 which provides help to B cells promoting division, class switching, affinity maturation and division into plasma cells.

Also activates eosinophils via IL-4 and -5.

120
Q

What are the functions of the T-helper cell Th17?

A

Helps the response to extracellular bacteria and fungi. They secrete IL-17, -21 and -22 which provide help at epithelial and fibroblast cell surfaces by promoting secretion of antimicrobial peptides and aiding in wound healing.

They also promote maturation of neutrophils and attract them to the site of infection via chemotaxis.

121
Q

What is autoreactivity?

A

When healthy cells presenting self proteins on their MHCI receptors get recognised by a CD8 t-cell and are killed.

122
Q

What is the role of immune tolerance?

A

Prevents autoreactivity but permits appropriate anti-pathogen responses.

123
Q

What happens when T-cells are maturing in the thymus?

A

1) Their TCR genes undergo gene rearrangement.
2) Both CD4 and CD8 receptors are presented.
3) Cells bind to either MHCI or II receptors on the thymic cortex. Those that bind to MHCII become CD4 and those that bind to MHCI become CD8.

124
Q

What happens to premature T-cells that do not develop properly in the thymus?

A

The cells that produce non-functional TCR receptors or do not bind to any MHC receptors in the thymic cortex die by apoptosis.

125
Q

How does negative selection to eliminate high affinity self-reactive T-cells work?

A

Special antigen-presenting cells called thymic medullary epithelial cells (TMECs) express MHCI & II. T-cells that do not bind with particularly high affinity to peptides expressed on the MHC receptors are allowed to go into the circulation. Those that bind with very high affinity are killed by activation-induced death.

126
Q

What are the peripheral mechanisms of immune tolerance?

A

1) Anergy = when T-cells receive signal one but not signal two.
2) Regulatory T-cells.

127
Q

Why is anergy important?

A
  • For tolerance to antigens not expressed in the thymus.
  • For tolerance to food antigens.
  • For tolerance to commensal (symbiotic) bacteria.
128
Q

What are the ways in which regulatory T-cells work?

A
  • Can stop T-cells from proliferating and prevent them from making cytokines.
  • Reducing co-stimulation and altering cytokine production by antigen-presenting cells which dampens the signal to T-cells.
129
Q

What are the two types of regulatory T-cells?

A

nTreg = produced in the thymus, respond to self-antigens and provides protection for autoimmunity.

aTreg = activated and developed from naive T-cells in the periphery, regulates response to food antigens provides protection for autoimmunity.

130
Q

What causes lymph nodes to become swollen in infections?

A

Mature/activated dendritic cells travel in the lymph to the lymph nodes where they secrete a combination of cytokines and chemokines which leads to an upregulation of adhesion molecules on the high endothelial venules that line the arterioles going into the lymph node. This leads to an increase in the migration of the naive T-cells into the lymph node.

The signals allowing the T-cells to move out of the lymph node are blocked which causes the swelling of the lymph nodes.

131
Q

What is the purpose of keeping naive T-cells in the lymph nodes when there is an infection?

A

They spend this time differentiating and proliferating and 5/6 days later they burst out of the node and migrate to the infection site having gained their effector function.

132
Q

What is the main difference between normal and memory T-cells?

A

The memory cells do not need the 5/6 days in the lymph nodes in order to proliferate and gain their effector function - they are able to respond immediately and differentiate.

133
Q

Define tissue repair.

A

The replacement of injured tissue either by regeneration (if the damaged parenchyma can divide and be replaced) or by fibroblastic or glial (within the CNS) scar tissue.

134
Q

What are the four cardinal signs of inflammation?

A 
Rubor = redness
Tumour = swelling
Calor = heat
Dolor = pain
135
Q

What are the vascular changes in the acute inflammatory response?

A
  • Initial transient vasconstriction of arterioles that lasts a few seconds followed by vasodilation and increased blood flow.
  • Then, slowing of the circulation because of increased permeability of the microvasculature. Sometimes the flow can stop completely and go into stasis.
  • The reduced flow causes tissues to become protein rich which leads to oedema.
136
Q

What is acute serous inflammation?

A

Where fluid accumulation has become the predominant feature of the immune response. This is seen in blisters and burns.

137
Q

What is exudate and where is it seen?

A

An inflammatory, extravascular fluid that has a high protein concentration and much cellular debris.

This is seen in acute inflammation.

Pus is a form of exudate.

138
Q

How do endothelial cells attract white blood cells in the blood during inflammation?

A

In response to factors such histamine and thrombosis factors, endothelial cells release adhesion molecules (P-selectin) from organelles called Weibel-Palade bodies which are then expressed on the cell surface and attract the neutrophils.

The neutrophils begin to roll along the endothelium.

This entire process is called MARGINATION.

139
Q

What happens after margination?

A

The neutrophils eventually lose momentum and become stationary. The inflamed and infected cells then release chemokines such as IL-8 which attracts neutrophils down a concentration gradient.

140
Q

What are the three main inducers of chemotactic agents for neutrophils?

A

1) Bacterial products
2) Components of the complement system (particulary C5a)
3) Products of the lipoxygenase pathway of arachidonic acid metabolism (particulary leukotriene B4)

141
Q

What is extravasation?

A

Movement of cells into tissues following the chemokine gradient.

142
Q

What happens if the presence of neutrophils is the predominant response to infections?

A

Acute suppurative inflammation = an enormous accumulation of pus.

143
Q

What is acute fibrinous inflammation?

A

Accumulation of fibrin in inflammation of the lungs.

144
Q

What is associated with chronic inflammation?

A

Infiltration by cells of the immune system (macrophages, lymphocytes and plasma cells) followed by proliferation of blood vessels (angiogenesis) and fibroblasts.

145
Q

What may chronic inflammation begin as and in what situations might this happen?

A

A low-grade smouldering response. The acute response is bypassed

This happens in persistent infections, prolonged exposure to non-degradable substance and autoimmune diseases.

146
Q

What are granulomas?

A

Macrophages with a cuff of lymphocytes.

They come in two types:
1) Non-caseating (non-infectious) epithelioid granuloma. They attract fibroblasts that produced collagen.

2) Caseating (infectious) epithelioid granulomas. These undergo central necrosis and also attract fibroblasts that produce collagen.

147
Q

What happens to granulomas after fibroblasts have started to lay down collagen?

A

Over about 8 weeks, they will replace the granuloma with a fibrous scar.

148
Q

Under which circumstances are granulomas seen?

A
  • When non-degradable foreign bodies are inhaled/ingested
  • Tuberculosis
  • Paraffin oil in the lungs
149
Q

What is immediate hypersensitivity also known as?

A

Allergy

150
Q

What is allergy mediated by?

A

IgE
Mast cells
Cd4+ Th2 cells

151
Q

What is atopy?

A

An inherited tendency to make immediate hypersensitivity responses.

152
Q

What happens immediately after a person encounters an allergen?

A

Mast cells degranulate and and release histamine causing a wheal (raised lesion) and flare (surrounding redness).

153
Q

How are Th2 cells activated in the immediate hypersensitivity response?

A
  • Antigen-presenting cells take up the antigen and presents their peptides on MHCII receptors.
  • CD4 cells recognises the MHCII receptors and the presented peptides which causes them to differentiate into Th2 cells.
154
Q

What are the actions of Th2 cells in the immediate hypersensitivity response?

A

They release IL-4, -5 and -13 which trigger B-cells to undergo class switching and differentiate into plasma cells that only release IgE antibodies.

155
Q

What happens to IgE when it is released from plasma cells in the immediate hypersensitivity response?

A

They bind to mast cells in the nose, skin or any other mucosal site.

When the allergen arrives, it binds to more than one IgE antibody (cross-linking) which provides a strong activation stimulus causing the mast cell to release its granular inflammatory mediator contents into the local tissue.

156
Q

What are common allergy diseases?

A
  • Asthma
  • Perinnial rhinitis (hayfever)
  • Allergic asthma
157
Q

What is desensitisation and how is this concept used in the clinic?

A

Where a person receives frequent doses of an allergen and their inflammatory response goes down.

In the clinic people are given controlled doses of the allergen they react to in order to cause desensitisation.

158
Q

Define autoimmunity and autoimmune disease.

A

Autoimmuninty = loss of immunological tolerance to self components.

Autoimmune disease = loss of immunological tolerance to self components associated with pathology.

159
Q

What are serum autoantibodies?

A
  • Usually IgG.

- They are used for monitoring disease activity and for predicting future disease.

160
Q

What two factors show proof of autoimmunity?

A

1) Passive transfer of disease by immune effectors (T-cells, antibodies). This is seen when Grave’s disease pathology is transferred to a foetus in pregnancy via placental IgG.
2) Clinical responsiveness to immune suppression or re-establishment of tolerance.

161
Q

What is seen in Grave’s disease?

A

An autoantibody is produced that binds to TSH receptors on the thyrocyte making it constitutively active. This means that thyroxine is being constantly produced by the thyroid without the negative feedback loop regulation.

Patients experience fast heartbeat, weight loss, bulging eye and a neck goitre.

162
Q

What is affected in myasthenia gravis?

A

Transmission across the neuromuscular junction is impaired due to an autoantibody that recognises the acetylcholine receptor.

163
Q

How was it proved that type 1 diabetes is T-cell mediated?

A

It was proven that a humanised monoclonal antibody against T-cells was an effective therapy to prevent beta-cell destruction.

164
Q

How do T-cells mediate type 1 diabetes?

A
  • The beta cells in the Islets of Langerhanns present their peptides directly on MHCI receptors which are recognised by CD8 cells which then kill the beta cells.
  • This is initiated when antigen-presenting cells take up beta-cell antigens and present their peptides on MHCiI receptors that are recognised by CD4 T-cells.
  • When activated, CD4 T-cells differentiate into Th1, Th17 and Th2 cells.
  • Th2 cells go on to stimulate B-cells to differentiate into plasma cells that produce antibodies that target the beta cells that are characteristic of the disease.
  • Th1&17 stimualte CD8 cells.
165
Q

How is the T-cell mediated action of type 1 diabetes allowed to happen?

A

Because there is a failure of Treg to suppress the autoimmunity.

166
Q

What are the two categories for immunodeficiencies?

A

1) Primary = inhertied = rare.

2) Secondary = acquired = common.

167
Q

What is Di George syndrome?

A

Where the thymus doesn’t develop so no T-cells can mature.

Example of a primary immunodeficiency.

168
Q

What is SCID?

A

Severe Combined Immune Deficiency.

Where T and B-cells fail to mature from lymphocyte precursors.

The ‘boy in the bubble’ suffered from this.

Example of a primary immunodeficiency.

169
Q

What is chronic granulomatous disease?

A

Where neutrophils fail to develop properly. They are circulating in the system but are unable to remove infections leading to an enormous inflammatory response.

Example of a primary immunodeficiency.

170
Q

What is hypergammaglobulinemia?

A

Also known as hyper IgM syndrome.

Where the CD40 ligand present on T-cells is abnormal so they are unable to simulate B-cells to differentiate into plasma cells. They are only able to produce IgM.

171
Q

What is the most common and well-known secondary immunodeficiency?

A

HIV

172
Q

How does HIV cause AIDS?

A

CD4 T-cells become infected through their receptor when they recognise and bind to antigen-presenting cells that are presenting the HIV peptide on MHCII. This infection causes the number of CD4 cells to decline.

Eventually, CD8 cells will recognise that the CD4 cells are virally infected and will start killing them. Unfortunately, this drastically reduces the CD4 cell population leaving the patient vunerable to diseases (AIDS).

173
Q

What is HAART?

A

Highly Active AntiRetroviral Therapy which is used to treat HIV.

174
Q

What is iatrogenic immune deficiency?

A

When patients are being treated with immune based therapies and they develop secondary immune abnormalities.

A reduction in the antibody that is causing the disease leaves the patient at risk to diseases and infections that are fought by the same antibodies.

175
Q

What are PD-L1 and PD-1?

A

PD-L1 = Programmed Death-Ligand 1 present on cancer cells.

PD-1 = Programmed Death-1 present on effector T-cells.

176
Q

What happens when tumours are treated with antibodies to PD-1 or PD-L1?

A

They stop the interaction between PD-1 and PD-L1 which ends the block on immune surveillance. This now allows the immune system to recognise and kill cancer cells.

177
Q

What are the three shapes of bacteria?

A

1) Bacilli = straight and rod-shaped.
2) Cocci = spherical shaped.
3) Spirilla = long and helical shaped.

These shapes are used to classify the bacteria.

178
Q

What are a) obligate aerobes; b) obligate anaerobes and c) facultative anaerobes?

A

a) Bacteria that are unable to respire anaerobically so must have an oxygen source.
b) Bacteria that are poisoned by oxygen so try to stay as far away from it as possible.
c) Bacteria that can respire aerobically or anaerobically.

179
Q

What are the most serious helminth infections caused by?

A

Tapeworms

Flukes

180
Q

What are the two stages of the life cycle of a protazoa?

A

1) Trophozoite = metabolically active growth stage.

2) Cyst = dormant stage.

181
Q

What are a) yeasts; b) hyphae and c) dimorphic fungi?

A

a) Single cell fungi
b) Branched filaments
c) Both single cell and branched

All three are types of fungi.

182
Q

What are fungi cell wall primarily composed of?

A

Chitin

183
Q

What are bacterial cell walls composed of?

A

Peptidoglycan

184
Q

Why do are some bacteria not stained with Gram staining? What staining is used instead?

A

Because they have an outer layer of complex, waxy lipids such as mycolic acids and the dyes used in the staining process don’t penetrate the wall. They are said to be acid-fast.

Ziehl-Neelsen (ZN).

185
Q

What is a bacterial capsule?

A

A gelatinous layer outside the cell wall mainly compossed of polysaccharides. They are antiphagocytic and helps bacterial adherance to host tissue in an infection. They are also antigenic.

186
Q

What are bacterial pili?

A

Also known as fibriae, they are hair-like filaments that extend from the cell surface.

They are more commonly seen in gram-negative bacteria.

187
Q

What are the two main functions of bacterial pili?

A

1) Attachment to host cells.

2) Sex pili are used in conjugation (mechanism in which bacteria exchange genetic material).

188
Q

What are bacterial plasmids?

A

Extrachromosomal double-stranded circular DNA molecules that are capable of replicating independently of the bacterial chromosome.

They contain information useful to bacteria such as antibiotic resistance and toxin formation.

189
Q

What are the three ways in which bacterial plasmids are transmitted?

A

1) Conjugation
2) Transduction
3) Transformation

190
Q

What bacteria produce spores?

A

Some gram-positive bacteria.

191
Q

What are bacterial spores composed of?

A

Bacterial DNA surrounded by a thick keratin-like coat that confers resistance to heat, chemicals and drying.

192
Q

What cell functions do viruses require to spread infection?

A
  • Machinery for translation of viral mRNAs
  • Enzymes for replication of the genome and assembly of new virons
  • Transport pathways to reach the sites of replication, viral assembly etc.
  • Energy source
193
Q

What are the three essential components of viruses?

A
  • RNA or DNA genome (never both)
  • Capsid core
  • Polymerase protein
194
Q

What are viral capsids composed of?

A

A small number of virally-encoded protein subunits called capsomeres.

195
Q

What are the three types of symmetry that viral particles show?

A

1) Icosahedral = 20 solid equilateral triangles arranged around the face of a sphere.
2) Helical = capsomeres are bound in a periodic fashion to the viral genome winding it to form a helix.
3) Complex = neither purely icosahedral or helical. Poxviruses are the only human viruses with this symmetry.

196
Q

How is the viral envelope attached to the viral capsid?

A

Through the viral matrix protein.

197
Q

What does the viral envelope determine?

A

The stability of virions outside the host and correlates with the mode of transmission.

198
Q

Are viruses that can survive in the environment (i.e. food or water) likely to have a viral envelope?

A

No

199
Q

What is the importance of viral surface proteins?

A

They are the target for antibodies in the immune response. Because of this, they are constantly evolving into different serotypes of the same virus to escape neutralisation.

200
Q

How is viral mRNA produced?

A

By transcribing the genome with host or viral RNA polymerase.

201
Q

What are the three types of symbiotic associations?

A

1) Commensalism = where one organism benefits and the other derives neither benefit nor harm.
2) Mutualism = association is beneficial to both organisms involved.
3) Parasitism = one organism benefits at the expense of the other.

202
Q

What are obligate intracellular parasites and what are faculative parasites?

A

Obligate =can only reproduce within host cells.

Faculative = do not rely on the host and can life and reproduce outside.

203
Q

What is immunopathogenesis?

A

Where the primary cause of death in infection is due to the killing of infected cells by the immune system not the pathogen itself.

204
Q

What are the four stages of infectious disease progression?

A

1) Incubation = the time between exposure and onset of a specific clinical sign.
2) Prodrome = the number of infectious agents starts to increase and the immune system starts to react characterised by non-specific symptoms such as fever, headache or loss of appetite.
3) Illness = active proliferation of the pathogen.
4) Recovery

205
Q

Define endemic, epidemic and pandemic.

A

Endemic = disease continuously present in a population.

Epidemic = disease with a greater number of cases than normal in an area for a short time i.e. an outbreak.

Pandemic = epidemic disease that has a worldwide distribution.

206
Q

What are the two types of persistent infections?

A

1) Latent = the microorganism persists after initial clearance and may have symptomatic or asymptomatic reactivation.
2) Chronic = infection takes years/will never be overcome (HIV). Pathogens continue to proliferate.

207
Q

What are nosocomial infections?

A

An infection acquired in a hospital or by a medical facility.

208
Q

What is the epidemiological triad?

A

The three factors that are essential for a disease to develop =

  • Host
  • Pathogen
  • Environment
209
Q

What are iatrogenic infections?

A

Factors that disrupt the body’s non-specific mechanical barriers to infection making it easier for microorganisms to invade.

  • Injury associated with an invasive therapy (surgery).
  • Plastic and metal foreign bodies (hip replacements, IV lines).
210
Q

What is virulence?

A

The pathogen’s ability to cause damage to the host.

211
Q

What happens when bacteria bind to host cells?

A

The bacterial adhesins mediate a series of signalling events that affect bacterial uptake and can promote inflammatory events by affecting innate immune receptors.

212
Q

What happens when a virus binds to a host cell?

A

The interaction of the virus with the receptor induces a conformational change that leads to membrane fusion and penetration.

213
Q

What are the roles of attachment factors in viruses?

A

They help to concentrate the viral particles at the cell surface.

214
Q

What defines the host range for viruses?

A

The interactions of viral proteins with the host cellular receptors.

215
Q

What is tissue tropism?

A

The different tissues within a given host that are able to be infected by the pathogen. Attachment is a factor that determines tissue tropism.

216
Q

What is invasiveness?

A

The capacity of a microbe to enter and damage a tissue.

217
Q

How do bacteria spread to deeper tissues?

A

Producing enzymes called invasins.

218
Q

What are some ways in which bacteria spread or avoid the immune system?

A

The production of the following enzymes (invasins):

  • Collagenase and hyaluronidase = degrades collagen and hyaluronic acid disrupting the epithelial basal lamina.
  • Coagulase = triggers the formation of a fibrin clot around bacteria as protection against phagocytosis.
  • Leukocidins = degrades white blood cells.
  • Hemolysins = degrades red blood cells.
219
Q

Define pathogenicity and virulence.

A

Pathogenicity is the ability of a microbe to cause disease.

Virulence is the degree of pathogenicity in a microorganism.

220
Q

What is LD50?

A

Lethal dose 50 = the number of pathogens that will kill 50% of an experimental group of hosts.

221
Q

What is ID50?

A

Infectious dose 50 = the number of pathogens that will infect 50% of an experimental group of hosts.

222
Q

What are endotoxins and exotoxins?

A

Endotoxin = present in the cell wall of gram-negative bacteria.

Exotoxin = proteins actively secreted by gram-positive and negative bacteria.

223
Q

What are attenuated viruses?

A

Mutated viruses that cause a reduced or no disease.

224
Q

What are viral virulence genes capable of doing?

A
  • Altering the ability of the virus to replicate.
  • Modify the host defense mechanism.
  • Enable to virus to spread to the host.
  • Act as toxic proteins.
225
Q

What are superantigens?

A

SAgs are toxins that stimulate the immune system by binding to MHCII molecules and stimulating a large number of T-cells.

226
Q

What is epidemiology?

A

The science that studies when and where diseases occur and how they are transmitted in a population.

227
Q

What is a chain of infection?

A

A concept used to explain how a patient can acquire an infection from another person. This information for an infection can be used by epidemiologists to develop strategies to prevent and control epidemics as the infection needs all 6 links in the chain to be successful so breaking one link will prevent the transmission of disease.

228
Q

What are zoonotic diseases?

A

Spread of an infection between animals and people.

229
Q

What are emerging diseases?

A
  • Unrecognised infections

OR

  • Previously recognised infections that have expanded into new ecological niches often accompanied by a significant change in pathogenicity.
230
Q

What is a fomite?

A

Objects or materials which are likely to carry infection, such as clothes, utensils, and furniture.

231
Q

What is vehicle transmission?

A

Where disease is transmitted via a medium such as water, food, air or body fluids.

232
Q

What is vector transmission?

A

Where disease is transmitted via animals that carry disease from one host to another. Insects are the most important animal vectors.

233
Q

What is biological transmission?

A

A form of vector transmission where the pathogen spends part of its life cycle in the vector (animal intermediate) and then is transmitted to the host through a bite.

E.g. malaria, rabies.

234
Q

What are the differences between vertical and horizontal transmission?

A

Vertical = between mother and child either in uterto across the placenta, during delivery or during breast feeding.

Horizontal = person to person transmission that is not between mother and offspring.

235
Q

What are Koch’s postulates?

A
  1. The microorganism must be found in
    abundance in all organisms suffering from
    the disease, but not in healthy organisms.
  2. The microorganism must be isolated from
    a diseased organism and grow in pure
    culture.
  3. The cultured microorganism should cause
    disease when introduced into a healthy
    organism.
  4. The microorganism must be reisolated
    from the inoculated, diseased experimental
    host and identified as being identical to the
    original specific causative agent.
236
Q

What are the differences between direct and indirect detection methods?

A

Direct = detection of a microbe or its products.

Indirect = detection for antibodies against the pathogen.

237
Q

What are the four types of medium used to culture bacteria?

A
  • Defined = when the exact chemical composition is known.
  • Enrichment = contain the nutrients required to support the growth of a wide variety of organisms.
  • Selective = only supports the growth of specific microorganisms.
  • Differential = distinguishes closely related microorganisms with the use of dyes or chemicals in the media.
238
Q

What are cytopathic effects?

A

CPE = the dramatic changes in appearance in cells that are infected by viruses.

239
Q

What are serological tests?

A

Tests used to determine the presence of antibodies in serum or microbial antigens in tissue or body fluid.

240
Q

How do serological tests work?

A
  • Paired sera samples are collected during the acute phase (5-7 days after onset of symptoms) and the convalescence phase (after 2-4 weeks).
  • Seroconversion must be seen (at least a four fold rise in specific antibody titre between the acute and convalescent samples) for a diagnosis to be made.
  • Presence of IgM but not IgG antibodies can be an indication of a current active infection.
241
Q

What are the disadvantages of serological tests?

A
  • Does not distinguish between previous or current infection.
  • Serological methods are retrospective.
  • Need a long time to collect the paired sera.
  • Does not work with diseases that produce clinical disease before the appearance of antibodies.
242
Q

What are the three types of antimicrobial drug?

A

1) Bactericidal = kills the bacteria
2) Bacteriostatic = inhibits growth of bacteria
3) Both 1 and 2

243
Q

What are the four major targets for antibiotics?

A

1) Cell wall synthesis
2) Plasma membrane function = disrupting membrane potentials
3) Nucleic acid synthesis
4) Protein synthesis

244
Q

What are the three targets for antiviral agents?

A

1) Attachment and entry
2) Nucleic acid synthesis
3) Assembly and building

245
Q

What are bacterial resistance strategies?

A
  • Preventing drug from reaching its target by reducing its ability to penetrate
    the cell
  • Inactivation of drug via modification or degradation
  • Expulsion of the drug from the cell via general or specific efflux pumps
  • Modification of the drug’s target site within the bacteria
246
Q

What is active immunity?

A

Immunity which results from the production of antibodies by the immune system in response to the presence of an antigen.

247
Q

What is passive immunity?

A

Short-term immunity which results from the introduction of antibodies from another person or animal. This includes maternal antibodies from mother to child in breastfeeding and through the placenta.

248
Q

Under which circumstances is passive immunity used?

A

When there is not enough time to wait for the body to create an active immune response or when there is no effective active vaccine or treatment.

This was used to treat the healthworkers who developed Ebola.

249
Q

What is herd immunity?

A

In contagious diseases that are transmitted from individual to individual, chains of infection are likely to be disrupted when large numbers of a population are immune or less susceptible to the disease.

The success of a vaccination programme depends on this.

FBS 2 (3 decks)

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