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Amy Somerville > INF1 - E. IMMUNE SYSTEM AND VACCINATION-COVERED > Flashcards

INF1 - E. IMMUNE SYSTEM AND VACCINATION-COVERED Flashcards

1
Q

what are foreign objects classed into

A

allogenic - within species
xenogeneic - between species ie. transplant/implant

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2
Q

what is an antigen

A
  • component of the foreign material that the immune system uses to recognise the foreign body
    ie - protein on surface of the cell
  • if there is an immune response to that antigen = immunogen
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3
Q

what is an epitope or antigenic determinant

A

specific part of antigen that immune system uses to recognise it
ie -amino acid sequence

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4
Q

what is innate immunity

A
  • non-specific
  • rapid
  • first line: physical barriers and chemicals ie. skin, mucosa, sebum (oil that protects skin’s surfaces and maintains pH of 5)
  • second line: immune cells (neutrophils, macrophages), complement, fever, inflammation, antimicrobial peptides, interferons etc
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5
Q

what is adaptive immunity

A
  • highly specific recognition of an antigen and generation of immunological memory
  • several hours/days
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6
Q

where do immune cells arise from

A

single pluripotent progenitor cell in bone marrow

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7
Q

where are B cells produced

A

bone marrow

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8
Q

where do T-lymphocytes differentiate

A

thymus gland

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9
Q

where are antibodies produced from

A

differentiated population of the B-lymphocyte (plasma cell)

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10
Q

what cells are involved in adaptive immunity

A

T and B lymphocytes

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11
Q

what cells are involved in innate immunity

A

monocytes
macrophages
dendritic cells
mast cell
complement protein
neutrophils
eosinophils
basophils
natural killer cell

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12
Q

what are the granulocyte cells

A

neutrophils
eosinophils
basophils

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13
Q

what do granulocytes do

A

phagocytose and destroy micro-organism (neutrophils, macrophages, dendritic cells) or
extracellularly kill the micro-organism (eosinophils, basophils, NK cells)

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14
Q

what happens to monocytes

A
  • they are activated to become macrophages (have different phenotypes - switch from pro-inflam to anti-inflam)
  • macrophages secrete molecules which destroy bacteria directly, recruit immune cells to site of infection, help control inflam response
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15
Q

what is phagocytosis

A
  1. cells recognise antigen
  2. engulf it, close it in phagolysosome (suicide bomb)
  3. granules fuse to release enzymes and reactive oxygen molecules (superoxide, hydrogen peroxide, nitric oxide) kill and break up the micro-organism in the phagolysosome
  4. phagocytes may display part of microorganism on their surface - APC for recognition by T-cells

innate and adaptive linked

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16
Q

what are complement systems

A
  • complex of plasma enzymes that enhance phagocytosis
  • release of antimicrobial chemicals and aid killing/lysis
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17
Q

how do phagocytes interact with their targets

A
  • biophysical
  • sugar residues (glycol, mannose) on surface
  • LPS, teichoic acid
18
Q

what is opsonisation

A

immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes

immune system components used:
- IgG (IgA)
- complement factors eg - C3b
- C-reactive protein

19
Q

how does the bacteria evade the hosts’ immune responses

A
  • cell wall components and capsules make it bigger so:
    limit access/binding of immune system components
    limit recognition by immune system
  • enzyme, toxins
    damage immune system components: antibodies, complement proteins
    directly damage cell membrane of WBCs etc
    limit/prevent activity of phagolysosome
20
Q

what is adaptive immunity

A
  • the body’s ability to mount a defence response to an invasion
  • requires time for body to recognise and start producing antibodies
21
Q

what are the 5 attributes of adaptive immunity

A
  • specificity: one antigen
  • inducibility: activated only in response to antigen
  • clonality: when activated, cells can proliferate and form identical cells of antibody
  • unresponsiveness to self: doesn’t act on body’s own cells
  • memory: of specific pathogens
22
Q

what is the cell-mediated adaptive immune response

A
  • against specific endogeneous antigens
  • involves T-cells mainly (and B-cells)
23
Q

what is the humoral adaptive immune response

A
  • against exogenous pathogens
  • involves production of antibodies and involves B-cells (maybe with T-helper cells)
24
Q

do the innate and adaptive immune systems work together

A

YES

25
Q

describe the antibody structure

A
  • 2 identical heavy polypeptide chains
  • 2 identical light polypeptide chains = variable, involved in antigen recognition (Fab domain)
  • Fc domain (constant) involved in eliminating the antigen eg - bound by cells of innate immune system
  • chains linked by disulphide bonding
26
Q

what produces antibodies

A
  • naive B-lymphocytes in blood
  • IgM molecules on cell surface of B-lymphocyte act, ready to bind to any invading antigen
27
Q

what happened when antigen binds to IgM molecules

A
  • specific B-lymphocyte clone undergoes repeated cell devisions
  • some daughter cells differentiate, supported by signalling from T-helper cells into plasma cells which secrete antibodies
  • some remain as B-lymphocytes and act as memory system
28
Q

5 types of antibody that form the humeral adaptive immune response

A
  • IgM - primary response of circulatory system
  • IgG - secondary response of circulatory system
  • IgA - involved in mucosal immunity
  • IgE - produced by mast cells and involved in inflammatory response
29
Q

what are the 3 effector functions so antibodies can remove antigens upon binding

A
  1. Neutralisation: steric hindrance of the interaction of toxins, viruses, bacteria with host cell surfaces
  2. Opsonisation: Fc domain serves as a receptor for the ‘killer cells’ (neutrophils, eosinophils, NK cells) Opsonins tag to pathogen
  3. Activation of complement cascade: facilitates neutralisation, opsonisation, leukocyte activation, membrane lysis of micro-organisms, clearance of antigen by cells in liver
30
Q

what is the aim of a vaccination

A

body makes memory cells

31
Q

what does vaccine development and implementation depend on

A
  • severity of disease
  • effectiveness and safety of vaccine
  • cost and impact of vaccine
  • public confidence of vaccine
  • ability to implement the programme
  • longevity of immunity
32
Q

what are live/weakened/attenuated vaccines

A
  • live (but weakened) micro-organisms to produce a similar reposes to a live infection
  • life-long immunity
  • person can become ill
  • micro-organism might replicate

Oral polio vaccine, MMR

33
Q

what are killed and component vaccines

A
  • dead/inactivated/attenuated components of microorganism (cell wall extracts/toxoid)
  • not life-long immunity
  • can’t cause disease
  • repeat booster vaccines needed

Diphtheria, Hep B, Tetanus

34
Q

what are DNA and RNA vaccine

A
  • genetic info encoding a pathogenic antigen is introduced into human cells and transcribed and translated by us to express the antigenic protein
  • genetic material eventually lost from body

Bird flu, Covid-19

35
Q

what is meningitis

A
  • infection of the meninges (in CNS) causing inflammation
  • caused by viruses or bacteria mainly
  • travel through blood, pass BBB
  • pathogenicity factors: capsules, adhesins, trafficked inside cells like macrophages
  • sepsis is caused when microorganisms enter blood with components of cell wall or toxins triggering a potent inflam response
36
Q

what is the most common type of bacteria which causes meningitis

A

Meningococcal sp. and Pneumococcal sp.

37
Q

describe Neisseria meningitidis

A
  • gram -ve diplococcus bacterium
  • part of natural flora at back of nose and throat
38
Q

pathogenicity factors of Neisseria meningitidis

A
  • capsule which resists lytic enzymes found in phagosome
  • pili/fimbriae
  • adhesion
  • attach and penetrate through mucosal epithelia
  • survive in blood and pass across BBB
39
Q

how is Neisseria meningitidis spread

A

nasal or oral droplets

40
Q

how is Neisseria meningitidis classed

A

according to composition of polysaccharide capsule (serogroup) ie - A, B, C, W135, Y, Z

41
Q

how was 4CMenB vaccine developed (for meningococcal B meningitis)

A
  • reverse vaccinology ie - what is the most interesting bit of the microorganism
  • genome sequence of bacterium was decoded to find proteins most likely to be broadly effective vaccine candidates
42
Q

why is it called 4C

A
  • 4 components on surface of meningococcal bacteria are highly immunogenic causing an adaptive immune response

Amy Somerville (70 decks)

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