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agents of infectious disease > 9-14 immuno > Flashcards

9-14 immuno Flashcards

1
Q

give 2 examples of extracellular pathogens

A

streptococcus pneumonia
clostridium tetani

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2
Q

what is a serotype?

A

a form of a bacterium that can be recognised specifically by characterised antibodies

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3
Q

how do s. pneumoniae and Haemophilus influenzae interact in the body?

A
  • they compete with each other
  • HI responds to competition by signalling the immune system to attack SP
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4
Q

how does clostridium tetani evade the immune system?

A

a typical dose of tetanospasmin is too small to produce an immune response

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5
Q

how does the parasite which causes african sleeping sickness evade the immune system?

A

the protozoan acquires a dense layer of glycoproteins that continually change, allowing the parasite to dodge an attack from the host’s immune system

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6
Q

is antigenic drift very rapid or very slow in HIV?

A

very rapid - it outpaces development of the immune system

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7
Q

how does flu rapidly evolve?

A

through recombination of its RNA segments

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8
Q

what is antigenic variation?

A

when a pathogen alters its surface proteins to avoid the host immune responses

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9
Q

how long does the primary adaptive immune response take to develop?

A

7-10 days

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10
Q

how long does the secondary adaptive immune response take to develop?

A

4-6 days

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11
Q

what is the blood brain barrier?

A

it is tight junctions around brain capillaries to separate circulating blood from the brain extracellular fluid

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12
Q

what are the main barriers used in the first line of the innate immune system?

A
  • skin
  • tight junctions between epithelial cells
  • acidic stomach pH
  • mucus layers
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13
Q

what cell intrinsic responses are used by the innate immune system?

A
  • pathogen induced phagocytosis
  • degradation of dsRNA
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14
Q

what specialised cells are used by the innate immune system?

A
  • professional phagocytes (neutrophils, macrophages)
  • natural killer cells
  • the complement system
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15
Q

is the innate immune response specific to particular pathogens?

A

no

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16
Q

what is the mucus layer made up of?

A

secreted mucins and other glycoproteins

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17
Q

what are defensins?

A

small, positively charged antimicrobial peptides which have hydrophobic or amphipathic helical domains

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18
Q

do defensins have antimicrobial activity?

A

yes

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19
Q

what organisms possess defensins?

A

all animals and plants

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20
Q

are defensins more or less active on membranes containing cholesterol?

A

less

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21
Q

what does the innate immune system recognise to produce an immune response?

A

they recognise pathogen-associated or microbe-associated immunostimulants
- these are present on pathogen cells but not on host cells

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22
Q

what classes of PAMPs are recognised by human cells?

A
  • peptidoglycan
  • bacterial flagella
  • lipopolysaccharide
  • mannans, glucans, and chitin from fungi
  • CpG motifs in bacterial or viral DNA
  • N-formylmethionine (fMet) used for bacterial translation initiation
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23
Q

what receptors in the body recognise PAMPs?

A
  • soluble receptors in the blood
  • cellular receptors
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24
Q

what is complement?

A

around 20 soluble proteins that are activated sequentially upon infection

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25
Q

what is the lectin pathway for complement?

A
  • it uses mannose and fucose binding proteins
  • proenzymes activate the next complement component by cleavage, resulting in an amplified proteolytic cascade to activate C3
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26
Q

what occurs in the alternative pathway for complement?

A
  • when a pathogen’s surface is encountered, other proenzymes activate C3
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27
Q

what happens when C3 is activated?

A
  • C3 is cleaved into C3a and C3b
    1 - C3a is produced - this attracts phagocytes and lymphocytes, stimulating inflammation
    2 - C3b is produced - this binds covalently to the pathogens plasma membrane
    3 - pathogen bound C3b simulates a local cascade of reactions (C5-C8) at the marked membrane
    4 - C9 is inserted into the membrane
    5 - a C9 pore (membrane attack complex) breaches the membrane
    6 - the pathogen lyses
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28
Q

what is toll?

A

a Drosophila transmembrane protein with a large extracellular domain with repeating motifs

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29
Q

what molecule do toll-like receptors bind? what is the effect of this?

A

PAMPs
- it signals to the nucleus, which results in gene transcription for inflammation

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30
Q

where are toll like receptors usually found in the body?

A
  • on the cell membrane of epithelial cells and macrophages, dendritic cells, and neutrophils
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31
Q

how does Neisseria Gonorrhoeae evade the innate immune system?

A
  • the capsule has no LPS
  • it takes sugars from the host immune system (including sialic acid) and presents these
  • it is resilient to bactericidal effects
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32
Q

what are the 3 major classes of phagocytes?

A
  • neutrophil
  • eosinophil
  • macrophages
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33
Q

which of the 3 classes of phagocytes are classified as granulocytes?

A

neutrophils and eosinophils

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34
Q

describe the main features of neutrophils

A
  • they are the most common type of granulocyte
  • short lived cells
  • abundant in blood
  • not present in normal healthy tissues
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35
Q

what recruits neutrophils to infection sites?

A
  • activated macrophages
  • peptide fragments of cleaved complement proteins
  • some PAMPs
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36
Q

what are the main features and uses of macrophages?

A
  • they are much larger and longer lived than neutrophils
  • they recognise and remove senescent, dead, and damaged cells
  • they are able to ingest large microorganisms such as protozoa
37
Q

what are the uses of eosinophils?

A

they help to:
- destroy parasites
- modulate allergic inflammatory response

  • they collectively recognise and kill cells with complement
38
Q

what recognises cell surface receptors displayed on phagocytes?

A
  • TLRs
  • receptors for antibodies produced by the adaptive immune system
  • receptors for complement C3b proteins
39
Q

what occurs when a receptor binds to a phagocytes cell surface receptors?

A
  • it activates phagocytes, enhances killing power, and causes cytokine release to attract more white blood cells
  • it induces actin polymerisation on the site - the phagocyte’s plasma membrane surrounds the pathogen to enguld if in a membrane-enclosed phagosome
40
Q

what are granules?

A

dense membrane-bound lysosomal derivatives

41
Q

what are the functions of granules in granulocytes?

A
  • they fuse with the phagosome membrane and release their contents to digest pathogen cell walls
  • granules also contain defensins to destabilise pathogen membranes
42
Q

what is a respiratory burst?

A
  • an increase in oxygen consumption
  • NADPH oxidase complexes form on the phago-lysosomal membrane, and a respiratory burst by phagocytes allows NADPH oxidase complexes to produce highly toxic oxygen derived compounds
43
Q

do neutrophils survive after phagocytosis?

A

no, they eject their own DNA to trap bacteria

44
Q

how do some bacteria resist respiratory bursts?

A
  • they survive and replicate inside the neutrophil by expressing virulence factors to protect against these bursts
  • e.g. Neisseria gonorrhoeae
45
Q

how do some bacteria resist actin polymerisation in phagocytosis?

A
  • they neutralise actin polymerisation by injecting a toxin that disrupts assembly of the actin cytoskeleton
  • e.g. Yersinia pestis
46
Q

how do sites of inflammation form?

A
  • blood vessels dilate leading to local swelling and the accumulation of complement cascade components
  • macrophages secrete cytokines which attract neutrophils
47
Q

how does the innate immune system recognise viruses?

A

it recognises:
- CpG motifs in viral DNA by TLR9
- viral dsRNA

48
Q

how are interferons produced?

A
  • IFN-alpha and IFN-beta are produced by all cells in response to viral dsRNA
  • IFN-gamma is produced by T cells when activated by their cognate antigen
49
Q

what are the main functions of interferons?

A
  • it warna neighbouring cells of infection and induces expression of other cytokines
  • it activates dssRNA nuclease which degrades host ssRNA non-specifically
  • it inhibits the process of translation in neighbouring cells
  • it limits viral spread by promoting apoptosis of the infected cells
  • it upregulates viral peptide display on infected cells to provide increased recognition by activated T cells
  • it stimulates expression of the immunoproteasome to process and destroy viral proteins
  • attracts natural killer cells and activates macrophages
  • fights cancers
50
Q

what are the functions of natural killer cells?

A
  • NK cells recognise cells with low expression of immune system recognition
  • they are also attracted to virally infected cells by IFNs and induce apoptosis
51
Q

define what is meant by an antigen

A

any substance capable of generating an adaptive immune response

52
Q

how does a vaccine cause immunisation?

A

1 - an antigen is injected in the form of a suspension containing adjuvant
2 - adjuvant activates innate immunity responses
3 - the activated innate responses also responds to the antigen in the vaccine
4 - the innate immune response then trains the adaptive immune response

53
Q

where do lymphocytes develop from?

A

in central lymphoid organs:
- bone marrow
- thymus

54
Q

where do lymphocytes migrate to after development?

A

to peripheral lymphoid organs:
- adenoids
- tonsils
- lymph nodes
- spleen
- Peyer’s patch (in the small intestine)
- appendix
- skin
- respiratory tract

55
Q

what are the main functions of dendritic cells?

A
  • they display a wide variety of TLRs
  • they phagocytose and degrade invading microorganisms
  • they display the peptides from the degraded organisms on their cell surface
  • they then migrate to a nearby lymphoid organ and activate the adaptive immune response
56
Q

how do T cells develop?

A

hematopoietic stem cells -> common lymphoid progenitor cells -> thymocytes -> t-cells
- occurs in the thymus, stem cells come from bone marrow

57
Q

how do dendritic cells activate T cells?

A

1 - DCs present peptides to T cells in the lymphoid organs
2 - T cell TCR recognises non self antigen and activated mitosis and clonal expansion of these specific T cells

58
Q

why do APCs only present to T cells?

A

1 - co-stimulatory molecules on APCs ‘dock’ with T cell specific co-stimulatory molecules
2 - the peptide is held in the groove of an APC and is scanned by the TCR

59
Q

what are the different classes of T cells?

A
  • T helper
  • T cytotoxic
  • T regulator/suppressor
60
Q

what are the functions of T helper cells?

A
  • they activate macrophages, dendritic cells, and B cells
  • they maintain cytotoxic t cell activity by secreting a variety of cytokines
61
Q

what is the function of T regulatory cells?

A
  • they inhibit the function of helper T cells, cytotoxic T cells, and dendritic cells
62
Q

what is the function of cytotoxic t cells?

A
  • they kill infected cells by persuading them to undergo apoptosis
63
Q

how do cytotoxic t cells induce apoptosis?

A
  • they secrete perforins which assemble and form a channel in the target cell wall
  • they secrete specific proteases which enter the target cell wall and activate caspases (the effector proteins of apoptosis)
64
Q

what do B cells differentiate into?

A
  • they differentiate into effector B cells (plasma cells)
  • they can secrete antibodies into the surrounding environment
65
Q

what is the basic structure of an antibody?

A
  • they are tetrameric with 4 polypeptide chains (2 identical heavy chains and 2 identical light chains)
  • the chains are held together by covalent disulphide bonds at the hinge and between the heavy and light chains
66
Q

how are classes of immunoglobulins distinguished?

A

by their heavy chains

67
Q

what 5 classes of Igs do mammals have?

A

IgM - mew heavy chain
IgD - delta heavy chain
IgG - gamma heavy chain
IgA - alpha heavy chain
IgE - epsilon heavy chain

68
Q

describe the basic structure of IgM

A
  • it is a pentamer of the basic tetrameric unit, held together by a joining chain to aid polymerisation
  • valency of 10
  • it is the first antibody a B cell makes
69
Q

what is meant by valency?

A

the amount of antigens a molecule can bind at one time

70
Q

which Ig class activates complement?

A

IgM

71
Q

what is an opsonin?

A

a molecule that targets antigens for phagocytosis

72
Q

describe IgG’s general structure and function?

A
  • has the standard tetrameric structure
  • IgM secreting plasma cells can switch to IgG secretion
    function:
  • toxin neutralisation
  • binding to microorganisms and opsonization by coating a pathogen and by activating complement
  • provision of passive immunity to fetuses and newborns
73
Q

how does IgG confer passive immunity?

A
  • placental cells take up maternal IgG by pinocytosis
  • placental endosomes have receptors that recognise and bind the tail region of IgG antibodies
  • the IgG molecules are transported across the placental cells in vesicles
  • IgG is released into the foetal circulation
74
Q

how is IgA secreted

A
  • IgM-secreting plasma cells can switch to IgA secretion
  • IgA is a dimer of 2 tetrameric units held together by a J chain, and also an S chain which allows secretion into saliva, tears, milk, and mucus
  • IgA protects our mucosal surfaces and provides some passive immunity to newborns via milk
75
Q

what is the basic function of IgE?

A

IgE binds Fc receptors on:
- mast cells
- basophils
- eosinophils

  • the bound IgE acts as a receptor for the particular antigen to which the original clonal expansion took place
76
Q

how and why does mast cell/ basophil degranulation occur?

A
  • triggered by IgE
  • results in a release of histamine at the site where mast cells and basophils meet the pathogen
  • histamines tigger blood vessel dilation and inflammation
77
Q

describe antibody structure at a domain level

A
  • light and heavy chains are composed of repeating Ig domains
  • the N-terminal domains of both chains are called variable domains
  • the remaining are constant domains
  • the antigen binding site is made from Vl and Vh domain interactions
78
Q

what is the structure of IgM?

A
  • there are multiple disulphide bonds and the H chain is heavily N-glycosylated
79
Q

what are the functions of the different domains in IgG?

A

CY1 and CY2 - bind complement components
CY2, CY3 - bind Fc receptors on neutrophils
CY3 - binds Fc receptor on macrophages and NKs

80
Q

describe the structure of IgE

A
  • the multiple N-glycans make this a stiff rigid molecule
  • good for targeting large pathogens
81
Q

describe the structure of IgA

A
  • very flexible, good cross-linker
  • valency of 4
82
Q

how do B cells become capable of class switching?

A
  • pre B cells in the bone marrow express IgM membrane bound
  • during maturation they express IgM and IgD, membrane bound in lymphoid tissue
  • the IgM+ IgD+ b cells are then selected by an antigen and undergo clonal selection
  • mature B cells can switch classes from igM to other Ig classes whilst maintaining the same specificity for antigen
83
Q

how does class switching occur?

A
  • via somatic recombination of DNA
    1 - the genomic DNA is looped so a recombination event can occur between sequences called switch regions
    2 - cutting and rejoining of DNA results in excision of the loop and class switching
    3 - the rearranged gene is transcribed to generate a primary transcript
    4 - the segments encoding Vh and Ca are fused in frame at the RNA level to generate mRNA
84
Q

define clonal selection

A

individual clones are selected by antigen based on how well the antigen and receptor fit together

85
Q

define clonal expansion

A

the selected clones undergo mitosis, proliferate, and differentiate into effector cells

86
Q

define clonal deletion

A

lymphocytes that react inappropriately with self antigens are destroyed

87
Q

how is primary antibody diversity generated?

A
  • the two classes of light chains increase diversity (lamda and kappa)
  • there are multiple gene segments encoding V domains that can be combined with C domains by somatic recombination
  • the somatic recombination used to select a V gene segment involves selection of small pieces of ‘diversity’ and ‘joining’ DNA to link the V domain with the constant domains
  • over time, the antibodies made by B cells improve in affinity and become more specific (affinity maturation)
88
Q

what is affinity maturation caused by?

A

an accumulation of point mutations in the V domains

89
Q

how does affinity maturation occur?

A

1 - antigen stimulation causes activation and clonal expansion of B cells with pre-existing fits to the antigen
2 - some B cells of the expanded clonal population proliferate in germinal centres and undergo somatic hypermutation, generating antibodies with altered V domain specificity
3 - most of these hypermutations are worse than the original so will not be stimulated by the antigen
4 - the rare b cell with mutation BCR versions that have higher affinity for the original antigen will proliferate resulting in rapid evolution of a high affinity antibody

agents of infectious disease (4 decks)

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