immunology (topic 2) Flashcards

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1
Q

antigen def

A

part of an organism/substance recognised as foreign so triggers the production of antibodies by lymphocytes

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2
Q

what substances do the immune system identify and fight

A

pathogens - biological agent causing harm/disease to the host
cells from other organisms of the same species - transplants
toxins
abnormal body cells like cancer

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3
Q

non-specific defence mechanisms - physical defences (7 of them)

A

skin = sebum is made of antibacterial fatty acids made by sebaceous glands, which waterproofs skin
mucus = lines airways, traps pathogens and are moved out lungs by coughing, sneezing, swallowing
cilia = waft pathogens/mucus in the respiratory system to the back of the throat to be swallowed
HCl = low pH denatures most pathogen enzymes
tears/salvia/urine = enzymes that hydrolyse proteins in pathogens
commensal microorganisms = compete with other pathogenic bacteria to prevent them colonising the body
reflexes = to close orifices when pathogens come at you eg being sneezed on

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4
Q

non-specific defence mechanisms - phagocytosis

A
  • phagocytes attracted to chemical products of the pathogen against a concentration gradient.
  • receptors attach to the pathogens cell surface antigens
  • lysosomes within the phagocyte migrate to the phagosome (formed by engulfing the bacterium)
  • lysozymes are released where they hydrolyse the bacterium
  • hydrolysis products are absorbed by the phagocyte
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5
Q

B lymphocytes info

A

formed from stem cells in bone marrow
mature in the bone marrow
associated with humoral response, respond to foreign material OUTSIDE body cells

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6
Q

T lymphocytes info

A

also formed from stem cells but mature in the THYMUS GLAND
cell mediated immunity / cellular response => respond to foreign material INSIDE body cells

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7
Q

B cell response (humoral response)

A
  • each has a unique receptor molecule on its surface membrane, BY CHANCE, one b cell will have a receptor with the complementary shape to the antigens on the pathogen
  • when the correct one binds, they multiply in response:
  • antigen moves by endocytosis into the b cell, which presents the processed antigens on its surface.
  • causes t helper cells to bind to the processed antigens and stimulate the b cell to divide by mitosis to form a clone of b cells with the same complementary receptor to the invading antigen (CLONAL SELECTION)

the cells of the clone differentiate => most become plasma cells that release antibodies (their receptors). some become memory cells (keep receptors) that remain in the blood for a long time after the pathogen has been destroyed

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8
Q

antibody def

A

proteins with specific binding sites, secreted by a B cell in response to a non self antigen

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9
Q

structure of antibodies

A

4 polypeptide chains - 2 heavy chains 2 light chains (quaternary proteins)
Y shape
variable region - antigen binding sites are different in different antibodies

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10
Q

why do immune system cells have specific molecules on its surface

A

proteins => have enormous variety, different sequence of amino acids —> different hydrogen bonds —> different shapes

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11
Q

antigenic variability

A

caused by random mutations, or have ability to switch proteins on and off to present different antigens to immune system

is a change in surface antigens (to help organism evade immune system of potential host)

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12
Q

antibody function

A

forms antigen-antibody complex
- causes AGGLUTINATION - each antibody has 2 binding sites, so they clump the bacteria together so phagocytes can engulf them more easily and faster
- serve as markers to stimulate phagocytes to engulf the cells the antibody has attached to

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13
Q

immunity def

A

ability of an organism to resist infection

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14
Q

passive immunity (external antibodies)

A

passive - transfer of antibodies to you that were produced by a different person. protection from this diminishes relatively quickly (few weeks or months)

  • no direct contact with pathogen necessary
  • provides instant response without waiting for primary immune response
  • relatively short lived (no memory cells)

eg anti-venom to snake bite victims, and antibodies passed to baby by mother

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15
Q

active immunity (your own antibodies) 2 types

A

body’s own immune system is stimulated to produce its own antibodies => takes time to develop but longer lasting

NATURAL active immunity - body produces its own antibodies AND memory cells and so is prepared for any future infection by the same pathogen

ARTIFICIAL active immunity - vaccination. immune system stimulated to produce immune response without you experiencing any symptoms of disease

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16
Q

vaccination def

A

introduction of a vaccine (antigen from a pathogen) to trigger an immune response and production of memory cells without inducing symptoms of a disease

17
Q

why vaccines are good

A

last for many years and initiate production of MORE antibodies FASTER

18
Q

what must a vaccine not do to humans and how

A

must be harmless to individual AND trigger immune response
done by:
- KILL pathogen (via heat treatment or chemicals, not too much that it denatures protein) so that antigens are unaffected eg cholera
- using bacterial toxins (an antigen) eg tetanus
- WEAKEN pathogen without affecting antigens eg polio (heat/chemicals)
- genetically engineered eukaryotic cells eg yeast, to produce microbial protein (antigen) eg hep B

19
Q

what makes a vaccination successful (and herd immunity)

A
  • quantity must be enough to vaccinate most of the vulnerable population
    => and enough to vaccinate vast majority of the population at the same time so susceptible people are indirectly protected as pathogen can’t spread (HERD IMMUNITY)
  • no unpleasant side effects
  • suitable means of storing/transporting vaccine - advanced tech, hygiene, refrigeration required
  • trained staff
20
Q

structure of a general virus - size, features

A
  • 50x smaller than bacteria
  • acellular
  • only able to replicate when inside a living cell
  • genetic material either DNA OR RNA, contained within a core
  • capsid protein coat
21
Q

HIV structure

A
  • spherical
  • envelope of lipids embedded in peg like attachment proteins
  • inside envelope = cone shape capsid containing 2 strands of RNA, and reverse transcriptase (enzyme)
22
Q

HIV being a retrovirus

A

can make DNA from RNA => reverse transcriptase

23
Q

infection with HIV, what happens (up to virus becoming active)

A
  • enters bloodstream
  • protein on HIV attaches to a protein called CD4 found on T helper cells
  • protein capsid fuses with T helper cell membrane, allowing viral RNA and enzymes to enter the cell
  • reverse transcriptase converts HIV RNA into DNA (HIV DNA)
  • DNA copy is moved into T helper cell’s nucleus and inserted into its DNA (now hiv positive)
  • every time cell divides viral DNA is copied as well. at some point virus dna becomes active and takes over the cell causing many more HIV viruses to be made
24
Q

how does it create new viruses

A

hiv dna in the T helper cell nucleus creates mRNA using the cell’s enzymes
this mRNA contains instructions for making new viral proteins to go into a new HIV virus
- uses some of the cell surface membrane as it’s lipid envelope
- this punctures holes in the membrane so water moves and cell dies, new infective HIV infects new T helper cells

25
Q

causes of symptoms of AIDS

A

T helper cells killed as the virus leaves, but may also be killed by other T cells in the cell mediated response as they are responding to cells infected with a virus
T cell number drastically reduced
- therefore B cells not stimulated to produce antibodies, memory cells may be infected + destroyed

immune response severely impaired, susceptible to opportunistic infections and cancers

26
Q

symptoms of AIDS

A

neurological => meningitis
eyes => retinitis
lungs => TB, pneumocystis pneumonia
skin => tumours
gastrointestinal => esophagitis

27
Q

ELISA test

A

well with antigens on it
wash surface to remove unattached antigens
add sample and leave to bind (if antibodies there, come into contact with hiv)
wash surface to remove excess antibody
add second antibody that binds with first antibody (2nd has enzyme attached)
add colourless substrate of enzyme (reaction colours it)
amount of antigen present relative to intensity of colour

28
Q

why are antibiotics ineffective against viruses like HIV

A

viruses lack metabolic processes - use host cells metabolic activity so antibodies can’t interrupt their metabolism
viruses lack cellular structure - antibiotics can’t disrupt these
viruses reside inside a host cell - antibiotics can’t reach them
viruses have a protein coat rather than murein cell wall - no attachment sites for antibiotics to bind to