c8- non test 1 Flashcards
1
Q
What are the two types of lymphocytes?
A
B lymphocytes (B cells- B for bone): fight bacteria: mature in bone marrow
T lymphocytes (T cells- T for thymus): mature in thymus
2
Q
Lymphocytes
A
look for mhc2 on the dendritic cell
- third line of defense
- third major group of WBCs
3
Q
What are dendritic cells?
A
-> Senses pathogen with receptors
-> Trigger production of cytokines, which attracts nearby dendritic cells to come help out and back them up
-> Kills pathogen, chews it down, display antigen on itself
-> Migrates to lymph nodes, and presents these antigens to T cells and B cells
-> This interaction triggers the activation of T cells and the production of antibodies by B cells, leading to a specific immune response against the invading pathogen.
4
Q
What two types of cells can monocytes develop into?
A
- dendritic cells
- macrophage
5
Q
What are macrophages?
A
- phagocyte cells which are larger and live longer than neutrophils
- also able to act as antigen-presenting cells
- has lots of vacuoles containing enzymes for digestion
- “big eater” (eats lots)
6
Q
Basophils
A
(0.01-0.3%) of WBC
- also involved in allergic reactions
- able to release histamine, thus helps to trigger inflammation
- able to release heparin, prevents blood from clotting
7
Q
Monocytes- when do they arrive?
A
- arrive at the latter stage of infection
8
Q
Eosinophils
A
(1-6%) of WBC
- involved in allergic reactions
- can attack multicellular parasites such as worms
9
Q
Three different forms of granulocytes
A
- Neutrophils
- Eosinophil
- Basophil
- named that way because they release granules
- all phagocytes-> ingest foreign cells such as bacteria, viruses and other parasites
- contains more neutrophil than anything else
10
Q
Three main groups of leukocytes
A
- Granulocytes
- Monocytes
- Lymphocytes
11
Q
specific/ adaptive immune responses
A
- produces memory cells that confirm long-term immunity to the specific foreign invader
- adaptive immunity includes both a HUMORAL RESPONSE produced by B cells- antibodies, and a CELL-MEDIATED RESPONSE produced by T cells that have the ability to destroy other cells
12
Q
Leukocytes: location and structure vs function
A
white blood cells
- normally circulate throughout blood, but will enter tissues if invaders are detected
- therefore can get to anywhere really fast
- many mitochondria to eat pathogens via active transport
- also lots of rough ER to form proteins
13
Q
Lymphatic system
A
- picks up everything that isn’t contained in the closed system- pushing them to the lymph nodes
- therefore when sick, they swell up- full of bacteria and other stuff
14
Q
What happens when a pathogen entered the body?
A
- A dendritic cell may eat it, chop it up, and stick its antigen(ponytail/ any substance that causes your immune system to produce antibodies against it) on the outside.
- Helper T cells come along and see if their antigen-binding site matches that specific antigen. There are hundreds of helper T cells with different antigen-binding sites, so this can take some time.
- Once the correct helper t cell with the exact antigen-binding site latches onto the dendritic cell, it becomes activated. 4. Meanwhile, B cells are floating around running into pathogens. If a B cell with the exact antigen-binding site latches to a pathogen, it gets little excited, but it waits until it’s fully activated by a helper T cell. (double check mechanism, so B cell doesn’t start attacking human cell.
- When the correct B cell is activated by the helper t cell, it replicates into two types of b cells: memory b cells and plasma b cells.
- Plasma b cells proliferate- make lots and lots of copies and start producing huge amounts of antibodies that have the exact antigen binding site for that pathogen
15
Q
Antibodies
A
Large protein molecules usually in a Y shape with antigen binding sites on the ends. These will latch onto a specific antigen from a specific pathogen.
16
Q
What are the two processes that antibodies go through?
A
Do several things
1. neutralisation- wrapping up the virus or the bacteria so they can’t do any damage
2. agglutination- stick big clumps of bacteria together until macrophage can come along and eat them
17
Q
natural killer cell
A
indiscriminate killers
- apoptosis
- innate
18
Q
Line 3: what are the 2 responses within it?
A
- humoral response-> B cells
- cell-mediated-> T cells
19
Q
antibody
A
wrap the pathogen to prevent them entering cells before macrophages come to eat them up
20
Q
Killer T-cells
A
Cytotoxic
- specific to one type of virus
21
Q
How do cytotoxic T-cells kill viruses?
A
Punch holes in the walls of invading virus-infected host cells, killing the cells and destroying the virus by injecting perforin and cytotoxic chemicals.
22
Q
Helper T cells- what are they
A
- cells designed to check if a human cell is healthy or infected with a virus
23
Q
How do cytotoxic t cells kill the specific viral cells?
A
- They do this by looking at the cell membranes and checking if they’re presenting healthy protein slices or viral protein slices(sliced-up bits of antigen stuck on the outside)
- you have hundreds of thousands of different killer t cells (cytotoxic t cells) which each have different antigen binding sites
- antigen-presenting cells such as a dendritic cell will slice up a pathogen and stick it on the outside of a MHC II molecule
- cytotoxic t cells will come past and check if their specific antigen binding site fits that particular antigen
- if it does it becomes activated but pauses for it to be confirmed by a helper T cell
- once activated by the helper t cell, it makes massive numbers of copies of itself, some of these are memory t -cells, which are stored to remember that particular virus
- others are suppressor t cells that switch the whole process off at the end of the infection
- but most are cytotoxic t cells released into the bloodstream
- activated cytotoxic t cells now roam the body checking cells MHC I complexes
- if it’s normal/ healthy, it presents self-antigens and the cytotoxic t cell will ignore it
- if it’s infected, it’s now producing viral DNA so it will put the viral antigen on its MHC I complex; that specific cytotoxic T cell will attach to the antigen, poke a hole in the cell membrane, and inject perforin, and cytotoxic chemicals which will kill the cell and the virus
- they can also cause apoptosis or programmed cell death
24
Q
Suppressor t cell
A
tells the body to settle down after all bacteria or virus-infected cells are killed, and stop making b cells and cytotoxic t cells.
25
E.g.s of immune system attacking itself
type 1 diabetes= immune system attacks pancreatic cells (islets of Langerhans) that produce insulin
multiple sclerosis
26
What's another word for specific immune system?
Adaptive immune system
Acquired immune system
27
Antigen
Chemical markers
28
What happens when you get hurt?
1. the first line of defense- the physical barrier has been penetrated.
2. damaged tissue releases histamines and other chemical signals which start the inflammatory response
a) this causes capillaries to become leaky, allowing fluid and white blood cells to get to the damaged area (not so much vasodilation)
b) hypothalamus increases temperature (fever)- increased metabolism to fight infection, burns off bacteria with lower optimal temperatures
c) fluid build-up causes swelling
d) white blood cells such as neutrophils and macrophages are called into the area, where they eat as much as possible. (neutrophils: 5-20 bacteria then die and become pus)
f) mast cells, or dendritic cells will take the pathogen, eat it, chop it up, and stick the antigen on its MHC II molecule, (an antigen-presenting cell)
3. You have millions of helper t cells, each helper t cell has a unique antigen-binding site.
a) Each helper T cell will see if its antigen-binding site fits the antigen from the antigen-presenting cell. This takes time to find a perfect match.
b) While this is happening, B cells with specific antigen binding sites are also checking the various antigens.
c) When a B cell finds an antigen that fits its antigen binding site exactly, it starts to get activated but then pauses.
d) The B-cell waits to be fully activated by the helper T cell (this is a double-checking mechanism to make sure your immune system doesn't fight human cells)
e) Once activated, the B cell multiplies into memory B cells (stored for later immunity) and plasma B cells
f) Plasma B cells mass produce millions of antibodies that flood the bloodstream and tie up pathogens with that precise antigen.
g) These are now stuck, can't do any damage, and await to be eaten by macrophages. As well as special lymphocytes and phagocytes that come to destroy them as well.
a) while this is happening helper T cells activate cytotoxic T cells with the precise antigen-binding site to making large copies of themselves as well.
b) the T cells divide into memory T cells (stored for later immunity), suppressor T cells (which switch off the immune response when the infection is over), and cytotoxic or killer T cells
c) These killer T cells roam the body, looking for infected human cells
- infected human cells will be producing viral protein or bacteria as a result presenting viral fragments on their MHC I molecule
d) A killer T cell that comes across a human cell with its own unique antigen fragment on the outside knows that is infected and needs to die.
e) The killer t cell kills the infected cell by poking a hole in the membrane injecting perforin and cytotoxins, which kills the cell and everything else inside it
f) it then just moves on to the next one and keeps killing
*When the infection is over suppressor t cells tell the immune system to stop more making more b&t cells and go back to normal
29
Where are mast cells located and why are they placed there?
- found in most tissues of the body, esp in locations that are in close contact with the external environment
- e.g. skin, airways, and intestines
- they are ideally placed to participate in the early recognition of pathogens-> first alert
30
The inflammatory response
"Not ok" signal= histamine
1. tells cells to dilate
2. tells wbc to stop rolling along and to come and fix it
3. capillaries dilate so blood supply is increased
4. capillaries become more permeable to scavenger wbc (squeeze thru membranes) and plasma proteins (help with repair)
- pyrogens are released
1. reach hypothalamus and the temperature rises (fever)= kills bacteria, may start to denature
2. more mucus, hence runnier nose or productive cough
3. pain receptors activate, sore joints or throat, body aches
4. WBC flock to infected area, neutrophils first
31
Mast cell: function
Once the mast cell detects damage, it releases granules and histamine to the surrounding area. This triggers an inflammatory response.
They also can eat some of the invading pathogens.
- call for help but also start the attack
32
Neutrophil
- most prevalent between the 3
- can ingest up to 5-20 bacteria in its lifetime
- become pus when they die
- attracted to chemotaxis (chemicals that attract cells to an area), e.g. histamines
- only last a few days in body before they self destruct, bone marrow produces more of them everyday
33
What happens when the first line of defence fails? Give an example.
- e.g. through a cut in skin, infection develops
The second line of defence becomes active:
1. inflammatory response
~ injured body cells releases chemicals, e.g. histamine that begin the inflammatory response
~ capillaries dilate so blood supply is increased (causing redness in skin and hotter)
- break down cytoskeleton to change its shape to fit in WBC
34
When a splinter enters the figure it often goes red and can produce pus. Explain in detail whar has happened to cause this and how it is linked to the immune system. Making reference to terms like Histamine, Neutrophils, and Pathogens. (5 marks)
When a splitter penetrates the skins it breaks through the first layer of deffence (1/2)
An imflamityory response is triggered (1/2)
Splinters often carry bacteria (1/2) that can now get access to damaged cells.
These bacteria are pathogens (1/2)
These damaged cells, in particular (mast cells) release Histomines (1/2)
Histamines increase blood flow to the area (1/2) make cappilaries leaky (1/2).
Blood will clot in the wound sealing it up (1/2)
This allows white blood cells like neutrophils (1/2) to slide through the capillary and engulf bacteria (1/2) these can eat about 5-20 then die and produce the pus (1/2) that appears at the injury.
As a result of the increased blood flow the area can become inflamed and sore (1/2)
35
Ducks (and many other water birds) have webbed feet that aid them in paddling.
a) Briefly outline how a population of ducks may have evolved webbed feet from an ancestrial population which did not have webbed feet according to Darwin's theory of evolution by natural selection. You may assume in your answer that there is a food source available in water which is easy to obtain relative to food on land.
(a) As a result of mutation, or meiosis and sexual reproduction a variation (1) in the degree of webbing of duck's feet arose. As more ducks are produced each generation than could survive to maturity some die due to competition (1) for resources. Since the food source in water was easier to obtain, the ducks with the greatest degree of webbing were able to obtain more (1) food. These ducks were more likely to survive (1), reproduce and pass this characteristic in to their
offspring (1). Ducks with webbing were selected (1) for, as they were better adapted (1) to their environment. The frequency of webbed footed ducks increased each generation (1).
36
Random exam questions q18
The sequence of five diagrams below show how pesticide resistance develops in a population of insects. Each insect symbol represents 10000 individuals. Assume there is no immigration or emigration.
Briefly explain, the steps in the development of pesticide resistance, (6 marks)
One mark allocated for each of the following points:
* Genetic variation in original population contains resistant genes, so a percentage of the initial population will be resistant to pesticide – due to random mutation;
* After first spray surviving population able to breed and transfer resistant genes to next generation – increasing % of resistant individuals;
* Following repeated spray there is a significant increase in the population of resistant flies;
* Pesticide is providing the selection pressure;
* Frequency of resistant genes is increasing significantly as a result of the selection pressure – actively being selected for..;
* End result is a population of insects in which a significant number carry the resistant gene – which will significantly lessen the impact of further sprays.
37
Random exam questions q9c
The common ancestor of the frogs was once widely distributed across Southern Australia. Changing sea levels and the drying of Central Australia geographically isolated the populations from each other (1), which prevented gene flow between the populations, isolating four different gene pools with their own variations (1).
The environments differed from each other, creating different selection pressures (1) and natural selection favoured the evolution of characteristics, which adapted each population to its particular environment and altered gene frequencies from the initial population (1).
Over time, the differences became sufficiently great to make Interbreeding impossible; the populations were reproductively isolated and speciation occurred, creating four new species from one (1).
38
Scientific names of organisms are often difficult to spell, pronounce and remember. Despite this, gardening shows on TV or radio, as well as gardening magazines, frequently use scientific names rather than common names for plants. Of what advantage is the use of sceintific names rather than common names? (2 marks)
Each species has a unique scientific name which is used internationally, so each organism's name is very specific and cannot be misinterpreted. (1)
Some organisms do not have a common name, so can only be referred to by their scientific name. (1)
As scientific names are in Greek/Latin, their meaning is not going to change over time, as will common names in other languages. (1)
Common names can cause confusion as several species have the same common name that may vary from region to region, or include unrelated species. (1)
Scientific names can convey information on features or distribution, or related organisms within the various groups with which it is classified. (1)
39
Some of the organisms in the food web feed on detritus. Explain the value of these organisms to others in the intertidal community. (2 marks)
Detritus, which is pieces of dead organic matter, contains many nutrients (1). Organisms which feed on detritus release these nutrients for reuse by other organisms within the community (1). Decomposers breakdown dead organic material and wastes, preventing their build up and producing inorganic nutrients and carbon dioxide for the producers. (1).
40
Random exam questions question 27 a,b
a) Penny tt (1)
Jim Tt (1)
Kevin Tt (1)
b) b) T roller, t non-roller
Geoff Anne
tt x Tt (½)
Gametes 1/1 t 1/2 T 1/2 t (½)
Genotype 1/2 Tt + 1/2 tt (½)
Phenotype 1/2 roller + 1/2 non-roller (½)
Chance child roller = 1/2
OR candidates can show punnet working (2)
t t
T Tt Tt
t tt tt
41
What evidence would biologists need to collect to determine that individuals in the Koala population (from different areas) are from the same species? (1 mark)
If individuals from different areas/populations can breed successfully, then by definition thay are the same species.
42
Once a macrophage has destroyed a gluten fragment, it displays a piece of the fragment on its membrane using a special major histocompatibility complex (MHC) marker. A T-helper cell then attaches to the MHC marker antigen complex. The macrophage T-helper cell complex is shown below.
The macrophage T-helper cell complex stimulates other cells and chemicals to target and damage epithelial cells that line the intestine. c.
Name one cell or chemical that would be stimulated by the macrophage T-helper cell complex and state its function. (2 marks)
Name___ cytotoxic T Cell (not B cell, as these are Celiac disease attacks epithelial cells of the small intestine) __Could also talk about Perforin or granzymes (chemicals used to cause cell death by cytotoxic cells).____________________________
Function: These cells find other cells that hold the same antigen and inject holes in the cell and cause apoptosis of the cells. This causes the symptoms of celiac disease.
43
Coeliac sufferers are unable to break down the gluten found in grains such as wheat. One of the features of celiac disease is ‘leaky gut syndrome’. A small gap appears between the epithelial cells that line the small intestine. Gluten fragments enter the gap and accumulate under the epithelial cells. Macrophages are stimulated to remove the fragments.
b. Explain how a macrophage is able to remove and destroy a gluten fragment. You may use a written answer or labelled diagrams or both. (3 marks)
Macrophage identify non human cells by looking at their Antigen on the MHC 1 molecule. If the antigen in not “self” then the macrophage consumes the invader by endocytosis. This is where the cell membrane envelopes the cell, wrapping it in a protecting membrane where lysosomes can come along and breakdown the contents with digestive enzymes. A diagram showing this would be good.
44
(b) Complete the following flow chart to show the immune response in a person receiving their first vaccination. The following words must appear in your flow chart.(3 marks)
Plasma cells memory cells B cells antibodies cytokines
The first step has been completed
Step 1
antigens detected by T-helper cells
Step 2:
Step 3:
Step 4:
(b) Step 2: T-helper cells produce cytokines to stimulate B cells
Step 3: B cells differentiate to produce plasma cells, which produce specific antibodies
Step 4: B cells also differentiate into memory cells
45
If the 2nd line defense was unsuccessful and the bacterium entered the blood stream, briefly explain what would happen next in terms of the immune response. (4 marks)
Third Line of Defence/specific immune response/acquired immune response/immune
response to specific antigens (½)
Macrophages engulf the bacteria and present the antigen on the surface (½)
Helper T-Cells sense the shape of the antigen (½)
Helper T-Cells release cytokines stimulating the proliferation of B/T cells (½)
B-Cells produce antibodies which attach to the antigen (½)
T-Cells kill infected cells with cytotoxic chemicals (½)
Memory T-Cell and Memory B-Cells are produced (½)
Remembering the antigen shape for future infections/quicker immune response next
time (½)
46
If the inflammatory response was occuring to you, identify and analyse the processes involved to explain how you would know it was occuring. (3 marks)
You would know it was happening because of redness, pain, heat and swelling at the
sight of infection (1) Mast cells release histamine (½) causes vasodilation and leaky
capillaries (½) vasodilation allows more white blood cells to enter site of infection
(½) increases blood flow and plasma to area which increases heat and redness pain
and swelling (½). White blood cells engulf bacteria and dead white cells result in pus
(½). Mentions of cytokine signalling to cells and pyrogens causing fever (½)
47
SWATVAC 2017 Qa
(a) Explain how the injection of antigens that Person B received caused the immune response shown in the graph. (3 marks)
The injection contained dead/inactive pathogen ( ½ ). On initial exposure to an antigen there are no antibodies present ( ½ ). However, the antigen triggers a specific immune response stimulating B cells to proliferate into plasma cells and memory cells ( ½ ). Plasma cells start producing antibodies but this proliferation takes several weeks (1) to build up enough antibodies to fight antigen. At 30 weeks the amount of antibodies decrease as the antigens have been destroyed by the body ( ½ ). The level of antibodies remains at a low level/ does not return to ‘0’ as memory cells (B and T memory cells) are still present to respond to re-infection ( ½ ).
48
SWATVAC 2017 Qb
(b) Explain how the immune response would differ if Person B was injected with the same antigens in week 50. (2 marks)
Antibodies are produced more rapidly ( ½ ) and in greater quantity ( ½ ) due to presence of memory cells (memory B and T cells) (1) produced during the primary exposure to the antigen.
49
SWATVAC 2017 Qc
(c) The immunity provided by the injection of antibodies into Person A was quite short-lived. Explain why. (2 marks)
The antibodies provided artificial passive immunity ( ½ ) to the antigen, that is, the person’s specific immune system was not triggered/stimulated ( ½ ) and as a result no memory cells were produced to replenish or replace the antibodies after a time period (1) so antibody levels decrease.
50
SWATVAC EVOLUTION B
(b) The long term survival of a species depends on having broad genetic diversity, so it is more likely to have variations which enable it to survive changing conditions (1). Using birds from both islets would give the broadest possible genetic base (1). Some of the genes important for survival on Floreana may have been lost from one, but not the other population, so using both would improve the survival chances of the re-‐established population (1). Another consideration is the possible negative effect of removing stock from the Champion island population that is probably at a critically low level (1).
Credit also given for: Gardner is a much larger island, and genetic drift occurs more slowly on larger islands as opposed to smaller islands, therefore use Gardner population, as more likely to still suit Floreana conditions (1).
3 well explained points.
51
SWATVAC EVOLUTION A
a) Yes, the 2 separate gene pools would vary (1⁄2), as these two populations are breeding in isolation/no gene flow (1⁄2). Plus two of the following: In each population different random mutations would occur (1); In each population natural selection occurs so that the birds become adapted to local conditions(1); In each population genetic drift randomly changes allele frequencies (1); The founding birds for each island may have had significantly different genetic make-‐ups (1).
Or
The habitats on the two islets would vary in food availability, vegetation, predators etc; leading to selection of those genes which best suited each population to its environment (1). Before birds were extinct on Floreana there may have been gene flow between the three populations, which limited the differences in genetic make-‐up (1). Once isolated the two remaining populations would have diverged genetically from each other. (1). This would also be influenced by the differences in populations between the islands and the mainland prior to Darwin’s time (1) and whether they had been totally reproductively isolated from each other over the recent times (1⁄2). Birds became adapted to local conditions.
52
Identify the main functions of monocytes, macrophages, and neutrophil.
A - Monocytes: Attend to infection sites causing inflammation and transform into
macrophages. (½)
B - Macrophage: Engulfs and digests infecting pathogens by phagocytosis. (½ )
C - Neutrophil: Leave the blood vessels and enter the surrounding cells to engulf pathogens.
(½ )
53
T-cells recognise and destroy disease-causing cells by binding to proteins on the surface of
the disease-causing cells.
Explain why T-cells can bind to proteins on the surface of disease-causing bacteria but
cannot bind to proteins on the body’s own cells.
(4 marks)
The immune system has the capacity to distinguish between its own body cells (self) and
foreign material (non-self)(½). All nucleated cells of the body possess the exhibit unique
molecules on their surface (1) (MHC)(½) which are recognized
T-cells are able to read/recognize the antigen proteins on the surface of all cells / markers
and determine if they are foreign or self. They are not equipped chemically with molecules
to bind to cells that are self but are able to bind to the foreign bacterial cells. (1½)
Sometimes the immune system identifies molecules of the self, as non-self. This case of
mistaken identity leads the immune system to attack itself, in what is termed an autoimmune
disease. (examples may be given) (1)
54
TASC 2021 Q26a
a) Identify the primary host of the liver fluke and explain what this means.
The human is the primary host because it is here that the larvae develop into adult flukes,
reproduce and produce eggs. (1)
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TASC 2020 Q21b
The graph below shows the concentration of antibodies in a patient’s bloodstream following
an influenza (flu) vaccination, and then a subsequent infection with the influenza virus.
Compare the immune responses that are taking place after the vaccination and after the
infection, explaining the differences between the two responses. (4 marks)
photos
56
TASC 2019 Q25c
Outline 3 important steps in how immunity is achieved through vaccination against measles, and explain why a booster shot is recommended. (5 marks)
photos
57
Tetanus is an infectious disease that can be fatal in humans. Commonly, people are
vaccinated to protect them from this disease. The following graph describes the
variation of the antibody level in a patient over a number of weeks. During this time two
separate vaccinations were administered.
With the first vaccination a new antigen enters the body, antigen-presenting cells (e.g. dendritic
cells) display antigens on their surface (½), activating helper-T cells which release cytokines (½)
to stimulate the immune system to produces B-cell (plasma cells) that make antibodies (½) and
T-cells that then specifically deal with the antigen presented (½). This means there is a ‘lag’
phase before antibody production increases (½). Memory B- and T-cells are also produced
that can recognise the particular antigen (½).With the second vaccination the antigen is
recognized (½) instantly so B and T cell production begins immediately (½) OR time course of response is much quicker (½). Overall antibody production reaches considerably greater
concentrations (½) and, once the pathogen has been dealt with, their concentration remains
higher (½).
58
After an individual is exposed to a microbial infection the body’s defence system
increases its activities.
The following graph summarises the timeline of the level of those activities.
Interpret the information from the graph above and explain why the different measures
of protection are effective over different time periods as well as physical distance from
the site of infection. (5 marks)
Physical barriers: initially such barriers as the skin, mucus etc. normally prevent the bacteria
from entry into body tissue (1/2). However, once breached (the site of infection), these
barriers are non-specific have no further role in defence (1/2). Very effective at providing
protection from pathogens continuously until barrier is breached (1/2).
Innate (non-specific) Immunity: Involves the inflammatory response (1/2) where
(macrophages/mast) cells that are disrupted caused chemicals/histamines to be released which
leads to vasodilation of blood vessels, increase in capillary permeability and influx of phagocytes
responding to destroy bacteria (1/2). This is also non-specific occurring close (1/2) to site of
initial infection and an immediate/fast response hence the sharp gradient in the graph (1/2). If
this response is not enough to destroy all pathogens (which may then invade other
tissue/blood/lymph) (1/2) then bacterial antigens can then be presented by phagocytes
(macrophages and dendritic cells) to helper T cells (1/2).
Acquired (adaptive/specific) Immunity: Helper T-cells would then become active to seek Bcells (or B/T memory cells) with an antibody match to the antigen (1/2) cloning of these
cells to facilitate a response. It takes at least 5 to 7 days to produce enough plasma B cells to
produce enough antibodies (1/2) to fight the pathogen so response is initially slow (1/2)
compared to the innate. Production of killer T-cells is also initially slow but proliferate to kill
already infected cells (1/2). Any B/T cells that recognise antigens will be further cloned to fight
infection increasing the response rapidly, but also leaving behind a memory to fight the
pathogen should it be encountered again (1/2). Proliferation of B and T cells occurs in the
lymph nodes which can be a much larger distance from the original entry point of the
pathogen (1/2). Specific immunity provides a much greater level of protection than the innate
system as it identifies the actual pathogen and produces an abundance of cells that work
together to fight the specific pathogen (1/2). Therefore, the further away from the site of
initial infection the pathogen becomes, the more specific the immune response becomes (1/2).
59
60
What are the two types of immunity?
Passive: antibodies gained in the placenta (N), antibody or T lymphocyte serum injections (A)
- getting immunity from someone else (e.g. mother passing immunity onto baby through placenta, protects them for a short period of time following birth, while immune system develops, lasts till antibodies die)
[immune system not doing anything, just injecting antibodies produced by someone else]
Active: acquired through actions of the immune system as a result of natural exposure to a pathogen (N) or through the use of vaccines (A) [follow full process of line 3]
- own immune system kicking in
(natural and artificial for both of them)
61
Active immunity
= you produce the antibodies
-> Your body has been exposed to the antigen in the past either through:
- exposure to the actual disease-causing antigen - you fought it, you won, you remember it
- planned exposure to a form of the antigen that has been killed or weakened (vaccine)- you detected it, eliminated it, and remembered it
62
How long does active immunity last?
- depends on rate of virus mutation
e.g. flu virus mutates quickly, therefore needs booster every year
- some stay basically the same, e.g. chicken pox (lifetime)
63
Herd immunity
stops the spread of disease totally if enough people are immune
- chances of spreading massively are low when there's only a small number of people with the disease
- not 100% vaccinated because not everyone can be vaccinated (weaker immunity, personal choice...)
64
Why can't 100% of the population be vaccinated?
- some allergic
- some weakened state (children, elderlies, cancer patients, etc)
- not ethical to force
65
Immune disorders
- mistakenly recognizes harmless foreign particles as serious threats
- launches immune response, causing sneezing, runny nose, watery eyes
66
What calms immune responses? (drug)
anti-histamines block effect of histamines and bring reief to allergy sufferers (stop mast cells)
67
AIDS
- specifically targets and kills t cells
- normal body cells are unaffected immune response is not launched
- stuffs up line 3 without initiating the whole thing
- resulting in the immune system not being able to function properly
68
Diagram:
Active natural: infection
active artificial: vaccination
passive natural: maternal antibodies
passive artificial: monoclonal antibodies
In reference to the diagram above, analyse the differences between the four types of immunity. (4 marks)
Active immunity is achieved when the body mounts an immune response that creates
memory B and T cells (½) and its own antibodies (½). This can happen naturally through
infection by a pathogen/antigen (½) or artificially through vaccination with a
weakened/inactivated/attenuated/killed version of the pathogen/antigen (½)
Passive immunity is when an individual is given the antibodies, without exposure to the
foreign antigen (½). This can happen naturally, when antibodies are transferred from mother
to child via breastmilk (or via the placenta) (½) or artificially where (monoclonal) antibodies
are injected/transfused into the recipient (½). In these instances, immunity is only
temporary/no memory cells are produced (½).
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If the non-specific immune response was not successful and the bacterium entered the blood stream, briefly explain what would happen next in terms of the immune response. (4 marks)
Third Line of Defence/specific immune response/acquired immune response/immune
response to specific antigens (½)
Macrophages engulf the bacteria and present the antigen on the surface (½)
Helper T-Cells sense the shape of the antigen (½)
Helper T-Cells release cytokines stimulating the proliferation of B/T cells (½)
B-Cells produce antibodies which attach to the antigen (½)
T-Cells kill infected cells with cytotoxic chemicals (½)
Memory T-Cell and Memory B-Cells are produced (½)
Remembering the antigen shape for future infections/quicker immune response next
time (½)
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explain why the image showed meiosis. (1.5 marks)
All show meiosis (gamete production) (½), presence of gametes (haploid cells) (½),
fertilisation (½) ( joining of haploid cells to form a diploid cell , zygote). All of which
are features of sexual reproduction.
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Poliomyelitis is an acute communicable disease of humans caused by human enterovirus polio virus transmitted between people. When it multiplies in the nervous system, the virus can destroy the nerve cells which activate the skeletal muscles resulting in paralysis. A polio virus infection can provide life low immunity against a visit. However, protection is limited to the strain of the disease a persons has had. In 1995, and inactivated polio vaccine was produced with all three strands of a disease, and since the global effort to eradicate polio has been underway.
describe how a person can acquire immunity *2 marks
When a person is exposed to the virus, It triggers a cell mediated response of the immune system. This is where a specific t cell with a specific receptor to the pathogen is triggered and goes around and kills any cell infected with that virus. the body then stores that specific T cell away (memory T cell), so if the virus is ever encountered again, it can respond quickly killing the virus before it does any damage. This is known as immunity.
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mucus membranes, such as those that line the respiratory system and digestive system, provide environment suitable for pathogen colonisation. describe how the body prevent pathogens from entering through these mucus membranes. include another mechanism that could be used in conjunction with the mucus membranes. (3 marks)
this is part of the first line of defence of the human body of physical barrier to entry. Any invading pathogens get stuck in the mucus. Tiny hairs called cilia beat in unison to move the pathogen out where they are sneeze out of the body. This is all designed to prevent pathogens entering the body at all.
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distinguish between active and passive immunity (2 marks
active immunity- when the body is exposed to a pathogen and develops its own immunity and memory of the attack so it can respond quicker next time.
passive- antibodies from someone else, mother or antibody donor, are injected into another person. They can attack a virus, but will only do so while injections are continued. Once they have stopped, the person has no immunity of their own.
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Some vaccines you need a booster injection. Using your understanding of the immune system, suggest the reason for why this might be needed. (2 marks
sometimes memory t and b cells wear off and are not remembered for as along, so the body needs a booster, another exposure to make more memory cells. or new variants might form.
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The first successful organ donation occurred in 1954, when an identical twin gave his brother a kidney. prior to that all organ transplants have been unsuccessful due to unseen biochemical factors. organ rejection was a continual problem until 1976, when it was discovered that cyclosporine was an effective immunosuppressant, since then, transplants have continued to have growing success around the world.
Explain why the early organ transplants were unsuccessful. (2 marks)
your body can identify self (antigens on the MHC 1 molecule) show that the cell is from its own body. A transplanted organ will have different antigens in the body immune system see it as a threat and start to kill off the organ. Hence It does not work.
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The first successful organ donation occurred in 1954, when an identical twin gave his brother a kidney. prior to that all organ transplants have been unsuccessful due to unseen biochemical factors. organ rejection was a continual problem until 1976, when it was discovered that cyclosporine was an effective immunosuppressant, since then, transplants have continued to have growing success around the world.
describe the importance of the discovery of cyclosporine and the impact on organ transplants since that time.
cyclosporine suppresses the immune system response. This means that immune responses weakened, so when the body recognises the new organ as foreign, it is not able to kill it off as it is not functioning as well as normal. This allows the organ to function as normal without being broken down in the body. as a result, you do not have to get an organ from a genetically identical person for the transplant to be a success.
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How does a vaccine work?
The process where the body is injected manually with a weakened or dead pathogen to induce antibody production so that this foreign antigen is successfully destroyed by the body's natural immune response. Future exposure to the pathogen will not cause disease, due to the production of memory t and memory b cells specific to the pathogen.
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Is vaccination immunity for lifetime? What decides this?
May be for a short time or for a lifetime, depending on the longevity of these memory cells.
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What's the difference between targets of humoral response and cell mediated response?
Humoral: targets pathogens themselves that entered the body with antigens displayed on their surfaces (e.g. fungi, bacteria, free viruses)
Cell-mediated: targets cells infected with a virus that displays viral antigen on their surfaces
