2C - The Immune System Flashcards

1
Q

What are antigens

A

Molecules (usually proteins) that generate immune responses when detected by the body.
- usually found on the surface of cells and used by immune system to identify..
Pathogens (organisms that cause disease)
Abnormal body cells (cancerous or pathogen infected cells - abnormal antigens on surface)
Toxins
Cells from other individuals of same species (transplants)

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2
Q

What are the first of four main stages in immune response

A
  1. Phagocytes engulf pathogens
    Phagocytes (eg. A macrophage) is a type of white blood cell that carries out phagocytosis
    —> engulfment of pathogens
    They’re found in blood and tissues
    And are first cells to respond to immune system triggers in body

— phagocytes recognise foreign antigens on a pathogen
— cytoplasm of phagocyte moves round pathogen, engulfing it
— Pathogen’s contained in a phagocytes vacuole (a bubble) in phagocytes cytoplasm
— lysosome fuses with phagocytes vacuole, lysozymes from it break pathogen down
— phagocyte presents pathogen’s antigens , to activate other immune system cells

diagram no.2

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3
Q

What’s the second of four main stages in immune response

A
  1. Phagocytes activate T cells
    —> T cells (T-Lymphocytes) is another type of white blood cell
    — has receptor proteins on its surface that bind to complimentary antigens
    Presented to it by phagocytes

This activates the T Cell; different t cell types respond in different ways.
Like t helper cells release chemical signals that
activate and stimulate phagocytes and cytotoxic T cells
—> cytotoxic t cells kill foreign and abnormal cells

T^h cells also activate B cells - they secrete antibodies

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4
Q

What’s the third of four main stages in immune response

A

T cells activate B cells (divide into plasma cells)
B cells/lymphocytes are a type of white blood cell,
covered with antibodies (proteins that bind antigens to form antigen-antibody complex)
- each B cell has a diff shaped antibody on its membrane
- so diff ones bind to diff shaped antigens

  1. When the antibody on the surface of the B cell
    meets a complimentary shaped antigen, it binds
  2. This with the substances released from t helper cells
    Activates B cell (clonal selection)
  3. Activated b cell divides into plasma cells
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5
Q

What’s the fourth of four main stages in immune response

A

Plasma cells make more antibodies to a specific antigen
- plasma cells are clones to b cell
- they secrete lots of antibodies specific to antigen (monoclonal antibodies)
- they bind to the antigens on the surface of pathogen to form antigen antibody complexes

An antibody has two binding sites
So can bind to two pathogens , meaning pathogens clump together (aggultination)
Phagocytes then bind to the antibodies
And phagocytosis happens to many pathogens at once

This process threads to destruction of pathogens carrying this antigen in the body

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6
Q

Antibody structure?

A

Antibodies are proteins - made up of amino acid chains
The specificity of an antibody depends on its variable regions (form antigen bind sites)

Each antibody has variable region with a unique tertiary structure (due to diff amino acid seq)
That’s complimentary to one specific antigen all antibodies still have the same constant region

diagram no.1

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7
Q

What can the immune response be split into

A
  • cellular response
    T cells and other immune system cells that they interact with
    Like phagocytes form cellular response
  • humoral
    B cells, clonal selection and production of monoclonal antibodies form humoral

Both types are needed to remove a pathogen from the body
And responses interact with each other
(Eg. T cells help activate B cells and antibodies coat pathogens making it easier for phagocytes to engulf)

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8
Q

What are the four steps of immune response diagram

A

Diagram no 3

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9
Q

What’s the primary immune response

A
  1. When antigen enters body for first time it activates the 8mmune system (primary response)
    - it’s slow because there aren’t many b cells that can make antibody to bind to it
  2. Eventually body will produce enough of the right antibody
    Meanwhile infected person will show the disease’s symptoms
  3. After being exposed to the antigen, t and b cells
    Will produce memory cells (stay in body for long time)
    — memory t cells remember specific antigen and will recognise second time round
    — memory b cells record specific antibodies needed to bind to antigen
  4. Person is now immune (immune system has ability to respond fast to a second infection by the same antigen/pathogen)
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10
Q

What’s the secondary immune response

A

If the same pathogens enters the body again ,
Immune response will be quicker and stronger (this is secondary)

— clonal selection happens faster.
— memory b cells (b-lymphocytes) are activated, dividing into
plasma cells that produce right antibody to the antigen

— memory T cells (t-lymphocytes) are activated, dividing into
correct T cell type to kill cell carrying antigen

Secondary response often rids of pathogen before symptoms show (you’re immune to pathogen)

diagram no.4
Is the graph of conc of right antibody in blood on both exposures

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11
Q

What exactly are memory cells ?

A

Memory cells are types of b and t lymphocytes
They just remain in blood longer than most t and b cells

When antigen enters body for a second time they can immediately divide
Into more specific b and T cells that can kill pathogen/release antibodies against

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12
Q

How do vaccines work to protect individuals/populations against disease

A

Vaccinations help avoid you suffering from disease
As b cells have to divide to build up numbers and deal with pathogen,
which takes a while meaning symptoms show
-
- vaccines have the antigens that cause your body to produce memory cells
- against that specific pathogen, without pathogen causing disease
Means immunity without symptoms

The antigens in the vaccine are free
OR attached to a dead/attenuated (weakened) pathogen

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13
Q

What is herd immunity

A

It’s where vaccines protect individuals that have had the vaccine
As well as reducing diseases’ occurrence
-> as those who aren’t vaccinated are less likely to catch disease
-> bc fewer ppl to catch it from

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14
Q

How are vaccines intaken

A

May be injected or intaken orally

Disadvantages of intaking orally
Are that antigens could be broken down by enzymes in gut
Or molecules may be too large to be absorbed by blood
- sometimes booster vaccines are taken later (years after)
- to ensure memory cells are still produced

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15
Q

What’s antigenic variation

A

It helps some pathogens evade the immune system
- antigens on pathogen surface activate primary response
- you don’t get ill during secondary response

  • however some pathogens change surface antigens (antigenic variation)
  • diff antigens are due to changes in genes of a pathogen
    This means that when infected for a second time, memory cells produced
    From first won’t recognise different antigens
    so immune system starts from scratch (another primary response with new antigens)
    —> Primary response takes time to rid of infection
    So you get ill again

Antigenic variation makes it difficult to make vaccines against some pathogens
Some are HIV and influenza virus

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16
Q

How does antigenic variation affect production of vaccines to prevent catching influenza

A

Influenza (flu) vaccine changes every year
As antigens change regularly (new strains of virus made)

Memory cells from vaccination with one strain of flu
Don’t recognise other strains (diff antigens)
—> strains are immunologically distinct

Different vaccine made each year for flu
Due to diff strains each year circulating population
New vaccines are developed and one is chosen every year
that’s most effective against recently circulating influenza
Governments and health authorities then implement
a programme of vaccination using suitable vaccine

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17
Q

Difference between active and passive immunity

A

Active
- type of immunity you get when immune system makes its own antibodies
- after being stimulated by an antigen
The two types of active immunity are
Natural: immune after catching disease
Artificial: immune after vaccine with harmless dose of antigen

.

Passive
- immunity gotten from being given antibodies made by different organism
- no antibodies produced of its own
The two types are
Natural: baby becomes immune due to antibodies from mother (placenta and breast milk)
Artificial: immune after injected with someone else’s antibodies - eg blood donations

18
Q

What are the differences between passive and active immunity

A

Active
- requires pathogen exposure
- takes a while for protection to develop
- memory cells made
- long term protection (antibody produced by memory cell activation
In response to complimentary antigen present in body)

.

Passive
- no exposure to antigen needed
- protection is immediate
- no memory cells
- short term protection as antibodies given are broken down

19
Q

What are monoclonal antibodies AND how are they made

A

These are antibodies produced from a single group
of genetically identical b cells/plasma cells
- antibodies are very specific because their binding sites
have unique tertiary struc (one antigen can fit with complimentary shape)

20
Q

How are monoclonal antibodies made to target drugs to cancer cells

A

Can be made to bind to anything you want (eg. Cell antigen)
Will only bind to this molecule only
1. Diff cells in body have diff antigens (eg. Cancer cells have
antigens called tumour markers - not found on normal body cells)
2. Monoclonal antibodies can be made to bind to tumour markers
You can also attach anticancer drugs to antibodies

  1. When antibodies come into contact with
    cancer cells they will bind to tumour markers
  2. Meaning drug will only accumulate (come together)
    on body where cancer cells are
  3. Side effects of antibody based drug are lower than other drugs
    As they accumulate near specific cells
21
Q

How are monoclonal antibodies used to target substance for pregnancy tests (medical diagnosis)

A

Pregnancy tests detect human chorionic gonadotropin (HCG)
in the urine of pregnant women (a hormone)
1. Application area has antibodies for HCG
bound to a blue coloured bead
2. When urine applied to application area any HCG
Will bind to the antibody on beads, forming an antigen antibody complex

  1. Urine moves up stick to test strip, carrying any beads with it
  2. Test strip has also antibodies for HCG stuck in place (immobilised)
  3. If HCG is present, test strip turns blue as immobilised antibody bind to HCG
    Concentrating the HCG Antibody complex with blue beads attached
    If no HCG is present, the beads will pass through test area without binding (won’t go blue)
22
Q

What’s the elisa test

A

(A medical diagnostic test that uses antibodies)
The enzyme-linked immunoabsorbent assay (ELISA)
Allows you to see if a patient has any antibodies to a certain antigen (or vice versa)
—> can be used as a test for pathogenic infections, for allergies
And for anything you can make antibodies for

In an ELISA test, an antibody is used wch has an enzyme attached to it
This enzyme can react with substrate to produce a coloured product
—> causes solution in the reaction vessel to change colour
— if there’s a colour change, an antigen/antibody of interest is there
— the quantity of antigen/body can be worked out from intensity of colour change

23
Q

What’s an example of an ELISA test

A

There are several types of ELISA
- direct elisa uses single antibody that’s complimentary to antigen tested for
- indirect elisa uses two diff antibodies

.

Indirect elisa can be used to see if a patient has antibodies to HIV

  1. HIV antigen is bound to bottom of well in well plate
    (A plastic tray with loads of little circular pits/wells in it)
  2. A sample of patient’s blood plasma (may contain several antibodies)
    Is added to well
    If any HIV specific antibodies, they will bind to HIV antigen
    Stuck to bottom of the well (wch is then washed out to remove unbound antibodies)
  3. A secondary antibody with specific enzyme attached is added to well
    Secondary antibody can bind to HIV antibody (primary antibody)
  4. Well is washed out again to remove any unbound secondary antibody
    (If no primary antibody in sample, secondary antibody will wash away)
  5. A solution is added to well (containing substrate able to react with enzyme attached to secondary antibody and produce a coloured product)
    - if solution changes colour, indicates patient has HIV antibodies
    - and hence IS INFECTED with HIV
24
Q

Why are washing steps important in elisa test

A

To ensure unbound antibodies aren’t left in well (may affect end result by making test appear positive at end even if no HIV antibodies present)

If the elisa test was negative there’d be no colour change as
There’d be no HIV specific antibodies for secondary antibodies to bind to

25
How is new knowledge about vaccines and antibodies validated by scientists (EXAMPLE) —> how to treat questions in exams
When one comes up with a new theory (eg. Vaccine has dangerous side effects), other scientists must come up with evidence to validate the theory. - other scientists may repeat study to reproduce the results - or conduct other studies to try to prove the same theory Eg. MMR vaccine 1. In 1998, a study was published on safety of measles, mumps and rubella (MMR) vaccine Study was based on 12 children with autism and concluded that there May be a link between MMR vaccine and autism 2. Small sample meant not everyone was convinced, increasing Likelihood that results were due to chance. - study may’ve been biased one of scientists was helping gain - evidence for a lawsuit against MMR vaccine manufacturer (Other studies found no link between autism and MMR. 3. there’s further scientific evidence to support conflicting evidence - a Japanese study investigated medical records of 30,000 children - born ‘88-‘96 (2005) and counted those diagnosed with autism before 7 - MMR was introduced in Japan at 89 and stopped in 93 (to those 12m old) . In exams, you’ll need to evaluate evidence like this.. DESCRIBE DATA - graph shows number of children diagnose with autism continued to rise after MMR stopped - for example.. (mention statistics) DRAW CONCS - no link between covariables. EVALUATE METHODOLOGY - sample was large, so results less likely to chance
26
What ethical issues are raised about vaccines and antibodies
Vaccines.. - treated on animals before humans, or animal based substances may be used to produce vaccines - testing on ppl is tricky (volunteers may be unaware of risk) - risk if side effects, but still protected through here immunity (some say it’s unfair) - a new disease would result in discussions like who’d be first to receive vaccine Monoclonal antibodies - animals produce the cells from wch monoclonal antibodies are produced
27
What is HIV
a virus that causes AIDS - HIV (human immunodeficiency virus) affects immune system Leadings to Acquired Immune Deficiency Syndrome (AIDS) - AIDS is where immune system deteriorates and eventually fails Making one vulnerable to other infections (eg pneumonia) HIV infects (eventually kills) t helper cells, acting as host cells for virus • Helper T cells send chemical that activate phagocytes, cytotoxic T cells and b cells • so they’re hugely important cells in immune response Without enough helper T cells, the immune system is unable To mount an effective response to infections As other immune system cells don’t behave how they shd AIDS is developed when t helper cell number reach critically low levels
28
What is HIV’s structure
— has genetic material (RNA) at its core and some proteins (including reverse transcriptase- an enzyme - for viral replication) — outer protein casing is the capsid — extra outer layer is the envelope (made of membrane stolen from cell membrane of previous host) — sticking out from the envelope are lots of copies of an attachment protein, wch help HIV attach to to host helper t cell **diagram no,5**
29
How does HIV reproduce
Viruses reproduce inside cells of the organism it has infected HIV replicated inside helper T cells of the host. - It doesn’t have the equipment like enzymes and ribosomes to replicate on its own - so uses host cells’ It replicates by.. 1. Attachment protein attaches to receptor molecule on Helper T cell membrane 2. Capsid is released into cell - it uncoats and releases its RNA Into cell cytoplasm 3. Inside cell, reverse transcriptase makes complimentary DNA strand From viral RNA template 4. From this, double stranded DNA is made, and insterted into human DNA 5. Host cell enzymes are used to make Viral proteins from viral DNA found in human DNA 6. Viral proteins are assembled into new viruses Wch bud from cell and infect other cells During initial infection period, HIV replicated rapidly and infected person May experience severe flu-like symptoms. After, HIV replication drops (latency period) - lasts for years, infected person doesn’t have any more symptoms
30
What do people with AIDS experience
Ppl are classed as having AIDS when symptoms of failing immune system appear Or helper T cell counts goes below a certain level - ppl with aids develop diseases that don’t cause serious problems in Those with a healthy immune system The length of time between infection with HIV and AIDS development varies But with no treatment, it’s about 10 years 1. Initial symptoms of AIDS are minor infections of mucous membranes Like inside ears, nose, and recurring respiratory infections 2. The, the number of immune system cells decreases more. —> patients become more susceptible to more serious infections Like chronic diarrhoea, severe bacterial infections and TB 3. In late stages of AIDS, patients have a very low number of immune system cells And can develop a range of serious infections like toxoplasmosis of the brain (a parasite infection) And candidates is of respiratory system (fungal) THESE kill AIDS patients, not HIV itself Length of time ppl survive with AIDS varies Factors affecting progression to AIDS and survival time are - existing infections - HIV strain infected with - age - healthcare access
31
Why don’t antibiotics work against viruses
Antibiotics kill bacteria by interfering with their metabolic reactions Targeting bacterial enzymes and ribosomes in these reactions - they are different to human ribosomes and enzymes - antibiotics are designed to only target bacterial ones so don’t damage human cells Viruses don’t have own enzymes or ribosomes, using hosts’ Antibiotics can’t inhibit them because they don’t target human processes Most antiviral drugs target virus specific enzymes (enzymes only virus uses) For example, HIV uses reverse transcriptase to replicate - human cells don’t use this enzyme so drugs can be designed for it without harming host (These drugs are reverse transcriptase inhibitors)
32
How is HIV treated
No cure or vaccine for HIV yet but antiviral drugs slow progression Of HIV into AIDS Best way to control HIV infection in populations is to Reduce spread (wch is through unprotected sex through infected bodily fluids) And from HIV positive mother to fétus - Not all babies from HIV positive mothers are born infected with HIV - And antiviral drugs in pregnancy can reduce chance of baby having HIV HIV testing in babies before 18m is inaccurate As baby of an HIV positive mother may have some antibodies In their blood even if not infected
33
Make fcs with key gems copy and paste
Yuh
34
How does the body recognise its own cells
Proteins (antigens) on the surface of cells allow the cells to be distinguished from one another. The immune system can identify: Pathogens Non self material such as cells from other organisms, toxins, cancer cells, cells infected by viruses
35
What happens when ymphocytes recognising own cells and bind accidentally (Thymus selection)
If the lymphocytes receptors fit with our own body cells, the lymphocytes will be deleted. These lymphocytes are suppressed or undergo apoptosis (programmed cell death). If they did not undergo apoptosis they would start to attack our own cells
36
How do phagocytes kill bacteria (phagocytosis)
Phagocytes killing bacteria: 1. Phagocyte attracted to bacteria by chemicals/ recognise antigens on bacteria as foreign; 2. Phagocyte attaches to antigens on pathogen. Engulf pathogen 3. Pathogen in vacuole / vesicle/phagosome 4. Lysosomes fuse with/empty lysozymes into vacuole: 5. Pathogen digested/hydrolysed 6. Pathogen antigens displayed on the phagocyte surface
37
Lymphocytes-2 types
-T cells- Mature in Thymus and are associated with cell mediated immunity -B cells- Mature in Bone marrow and are associated with antibodies/humoral immunity (memory and plasma cells). -Memory cells carry an immunological memory of the specific antigen. Plasma cells produce antibodies
38
Cell mediated immunity?
1. Pathogen displays antigens on surface 2 Pathogen taken up by phagocyte and antigen presented on surface 3 binds with receptor on specific T helper cell 4 this activates other T cells (by releasing cell signals called cytokines) 5. (divides to) form clones By mitosis 7. Cloned T cells stimulate phagocytes to engulf pathogens by phagocytosis AND stimulate B cells to divide into memory and plasma cells by mitosis (plasma cells make antiobdies) AND stimulate cytotoxic T cells to divide and kill infected cells (by making holes in the cell surface with perforin
39
Antibodies and their protein structures (quaternary structure)?
proteins that are specific to/complementary shape to antigen (produced by B cells/secreted by plasma cells). Due to tertiary structure. Made in body after infection Made of 4 polypeptide chains (quaternary structure) - Disulphide bridges join two different polypeptides together. - Binding site is the variable region (2 on each antibody), complementary to only one antigen. - Constant region binds to receptors on B cells
40
What’s agglutination and markers
Agglutination- clumps of bacterial cells are formed making it easier for the phagocytes to locate them. Markers - Stimulating phagocytes to engulf the bacterial cells to which the antibodies are attached.
41
What’s the humoural response (associated with b cell immune response)
1. Antigen presenting cell presents antigen on its surface 2. Binds with receptor on specific T helper cell 3. T helper cell releases signals called cytokines which activate B cells. 4 B-cell now divides by mitosis to form a clone of identical B cells (clonal selection) 5. Cloned plasma cells secrete antibodies 6. Some B cells develop into memory cells. They respond to future infections by dividing rapidly and developing into plasma cells that produce the specific antibodies faster.(secondary immune response)
42
How do vaccines work
1. Contain antigens/DNA/antigens are injected; 2. Antigen detected by phagocytes and display antigens 3. Antigens bind to receptor on a specific T helper cell/phagocyte 4. T cells releases cytokines 5. Stimulates B cells to divide by mitosis and make clones 6. Plasma cells (from b cells) make antibodies 7. Some B cells become memory cells 8. On second exposure memory cells produce antibodies more rapidly and in greater numbers