Cell Recognition And Immune System Flashcards

1
Q

What is immunity

A

Immunity - bodys ability to rapidly destroy before symptoms

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2
Q

What is a lymphocytes

A

If a pathogen gets past the chemical and physical barriers (e.g. skin and stomach acid) and enters the blood then the white blood cells are the second line of defence.

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3
Q

What is specific defense?

A

Specific —> can distinguish between different pathogens. Take slower to start but give longer lasting protection. Involves lymphocytes.

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4
Q

What is a non specific defence

A

Non-specific —> do not recognise individual pathogens. Offer a quicker response in earlier stages of infection. Involves phagocytes and physical barriers.

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5
Q

What is direct damage?

A

some pathogens attatch to your cells and tissues when they are released.

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6
Q

What is indirect damage?

A

Indirect - waste products released from some pathogens are often toxic to the host and therefore cause disease

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7
Q

How can our body identify self and nonself cells

A

• glycoproteins that act as a receptors on our cells plasma membranes signpost our cells as self.
• These receptors will be different to those of a nonself organism.
• The protein receptors on a pathogen are often referred to as antigens.

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8
Q

What is a phagocyte and what is phagocytosis?

A

A phagocyte is a macrophage (type of white blood cell) that carries out phagocytosis.
They are found in the blood and in tissues.
Phagocytosis is a non-specific response. Any non-self cell (e.g. pathogen) that is detected will trigger the same response to destroy it.

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9
Q

First four stages of phagocytosis

A
  1. Phagocytes are in the blood and tissues and any chemicals or debris released by pathogens or abnormal cells attract the phagocytes and they will move towards these cells.
  2. There are many receptor binding points on the surface of phagocytes. They will attach to chemicals or antigens on the pathogen via these receptors.
  3. The phagocyte changes shape to move around and engulf the pathogen.
  4. Once engulfed the pathogen is contained with a phagosome vesicle.
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10
Q

Last four stages of phagocytosis

A
  1. A lysosome within the phagocyte will fuse with the phagosome and release its contentz
  2. The lysozyme enzyme is released into the phagosome. This is a lytic enzyme which hydrolyses the pathogen.
  3. This destroys the pathogen.
  4. The soluble products are absorbed and used by the phagocyte
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11
Q

What is passive immunity

A

Antibodies are introduced into the body.

The pathogen doesn’t enter the body, so plasma cells and memory cells are not made.
No long-term immunity.
e.g. antibodies passed to a fetus through the placenta or through breast milk to a baby.

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12
Q

What is active immunity

A

Immunity created by your own immune system following exposure to the pathogen or its antigen
Natural active immunity
Following infection and the creation of the bodies own antibodies and memory cells
Artificial active immunity
Following the introduction of a weakened version of the pathogen or antigens via a vaccine.

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13
Q

lain why the number of HIV particles in the blood
(i) rises during the first few months after infection
Then
Remains low between 1 and 7 years after infection.

A

HIV is invading cells which make new viruses;
Cells release viruses into blood;

(ii) Virus remains dormant/exists as provirus/exists as DNA in host DNA;

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14
Q

What is a vaccine

A

Small amounts of weakened or dead pathogen, or antigens are introduced in the mouth or by injection.

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15
Q

What are B Cells role in vaccines

A

Exposure to the antigens activates the B cell to go through clonal expansion and differentiation (clonal selection)
B cells undergo mitosis to make large numbers of cells, these differentiate into plasma cells or memory B cells.
Plasma cells make antibodies
B memory cells can divide rapidly into plasma cells when re-infected with the same pathogen to make large numbers of antibodies rapidly.

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16
Q

What are memory b cells

A

These can live for decades in your body, where as plasma cells are short lived.
Memory B cells do not make antibodies, rather they will divide by mitosis and make plasma cells rapidly if they collide with an antigen they have previously encountered.
This results in large numbers of antibodies being produced so rapidly that the pathogen is destroyed before any symptoms can occur.
This is active immunity

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17
Q

What is herd immunity?

A

If enough of the population are vaccinated the pathogen cannot spread easily amongst the population.
This provides protection for those who are not vaccinated e.g those with already too ill to have a vaccine, or have lowered immunity unable, or those who are too young

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18
Q

What is histamine

A

• Causes inflammation
• Causes capillary walls to become more permeable so that they lose more fluid to the surroundings.
• Speeds up the delivery of phagocytes to the site of infection.

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19
Q

What are lympocytes and the two types?

A

Lymphocytes are white blood cells involved in the specific immune response.
All lymphocytes are made in the bone marrow, but T cells mature in the thymus.

• T Lymphocytes - cell mediated immunity (specific cells not antibodies)
• B Lymphocytes - humoral immunity (have antibodies in fluid in blood)

The cell mediated response is the response involving T-cells and body cells.

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20
Q

What do T cells do

A

Stage of immunity is specific and occurs in response to non-specific methords
Self cells that carry the pathogen antigens are recognised by Tcells and dealt with accordingly

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21
Q

What are antigen presenting cells.

A

Any cell that presents a non-self antigen on their surface:
• Infected body cells will present the viral antigens on their surface
• A macrophage which has engulfed and destroyed a pathogen will present the antigens on their surface
• Cells of a transplanted organ will have different shaped antigens on their surface compared to your self-cell antigens
• Cancer cells will have abnormal shaped self-cell antigens.

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22
Q

Why are cell responses called cell mediated

A

Cell responses are described a ‘cell-mediated’ because T cells only respond to antigens which are presented on cells (APC), and not antigens detached from cells and within body fluids, such as the blood.

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23
Q

First four stages of cell mediated response

A

1.One of the millions of specific T cells in the body will recognise and bind to the antigen being presented on the antigen-presenting cell membrane.

  1. The T cell will begin to divide to make millions of clones
  2. Some clones will stimulate phagocytes to phagocytose the pathogen
  3. Others (killer tcells) will kill the antigen presenting cell in order to get the pathogen.
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24
Q

Last four stages of cell mediated response

A
  1. T cells do this by releasing a protein that punctures the antigen presenting cell membrane
  2. Once punctured the membrane is no longer selectively permeable and will lose osmotic pressure. It will die along with the infecting pathogen/antigen
  3. Other t cell clones will enter the blood stream and circulate around the body looking for other pathogens expressing the same antigens.
  4. These memory cells will remain in the blood stream and are what allow our bodies to remember infection
  5. This immunological memory means that repeat infections of the same pathogens are dealt with before an infection manages to take hold.
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25
Q

Step one of miss estricj mediated response

A

. Once a pathogen has been engulfed and destroyed by a phagocyte, the antigens are positioned on the cell surface.
This is now called an antigen presenting cell (APC)

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26
Q

Step 2&3 of miss estricj mediated response

A
  1. Helper T cells have receptors on their surface which can attach to the antigens on APC.
  2. Once attached this activates the helper T cells to divide by mitosis to replicate and make large numbers of clones
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27
Q

Step four miss estrich cell mediated response

A
  1. Cloned helper T cells differentiate into different cells
    • Some remain as helper T cells and activate B lymphocytes
    • Some stimulate macrophages to perform more phagocytosis
    • Some become memory cells for that shaped antigen
    • Some become cytotoxic T cells (killer T cells)
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28
Q

What are cytotoxic tcells

A

Cytotoxicc T cells destroy abnormal or infected cells.
They release a protein, perforin, which embeds in the cell surface membrane and makes a pore (a hole) so that any substances can enter or leave the cell.
This causes the cell death.

This is most common in viral infections because viruses infect body cells.

Body cells are sacrificed to prevent viral molecule replication.

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29
Q

What is the humoral response?

A

The humoral response is the response involving B cells and antibodies.
Antibodies are soluble and transport in bodily fluids. ‘humour’ is an old term for body fluids, hence the name humoral response.

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30
Q

What are B lymphocytes

A

Produce antibodies
Millions of different types of B cells
Each distinct B lymphocytes is specific to a certain antigen like T cells.
Each specific B lymphocytes produces a specific antibody to a specific antigen.

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31
Q

What are the two types of B Cells?

A

Plasma cells - secrete antibodies against the specific antigen that activated it.
Memory Cells - circulate in the blood looking for a specific antigen. Once found they will turn into plasma cells which are a long lived response.

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32
Q

What is immunilogical memory?

A

if memory cells specific to a certain pathogen are already present in large numbers, then the cloning of lots of new lymphocytes is not required should the pathogen be detected again.

This means that the secondary response is much faster than the primary response so much so sometimes the individual doesnt suffer.

33
Q

B cell activation pafrt 1

A

A B cell is triggered when it encounters its matching antigen.
The B cell engulfs the antigen and digests it. Then it displays antigen fragments bound to its unique MHC molecules.

This combination of antigen and MHC attracts the help opf a mature mathing TCell
This

34
Q

Part two of B Cell antigen

A

Cytokines secreted by the TCell help the b cell to multiply and mature into antibody producing plasma cells.

Released into the blood antibodies lock onto matching antigens.
The antigenantibpdy compleced are then cleared by the comp;ement ascase or by thr liver and spleen

35
Q

How are b cells activated

A

Antigens in the blood collide with their complementary antibody on a B cell. The B cell takes in the antigen by endocytosis and then presents it on it’s cell surface membrane.
When this B cell collides with a helper T cell receptor, this activates the B cell to go through clonal expansion and differentiation (clonal selection)
B cells undergo mitosis to make large numbers of cells, these differentiate into plasma cells or memory B cells.
Plasma cells make antibodies
B memory cells can divide rapidly into plasma cells when re-infected with the same pathogen to make large numbers of antibodies rapidly.

36
Q

What is agglutination

A

Antibodies can cause microbes to stick together. This makes it easier for phagocytes to engulf them
Antibodies are flexible and can bind to multiple antigens to clump them together.
This makes it easier for phagocytes to locate and destroy the pathogens.

37
Q

What is the opponisation/compliment cascade

A

The binding of an antibody to the surface of the pathogen can set of a chain reaction with blood proteins causes pathogens to swell up and burst because osmosis occurs. As proteins have opened letting water into the cell.

Virus have proteins opn their surface which recognise and bind to receptors on surface of the host cell. This is how virus enter the host cell.

Antibodies can bind to viruses and stop them attaching to their host cell.

38
Q

What is nuetralisation

A

• pathogens make us ill by producing toxins
• Some antibodies work by nuetralising these toxins.

39
Q

How does your body identiy self and nonself cells

A

By cells and lymphocytes

40
Q

how can lymphocytes distinguish between pathogens and self-cells?

A

Each type of cell has specific molecules on its surface that identify it. These molecules are usually proteins, as their 3D tertiary structures enables lots of unique and identifiable shapes to be made.

41
Q

What can different surface molecules identify

A
  1. Pathogens (e.g. bacteria, fungi or viruses such as HIV)
  2. Cells from other organisms of the same species (harmful for those with organ transplants)
  3. Abnormal body cells (e.g. cancer cells)
    50 seconds
  4. Toxins (some pathogens release toxins into the blood, such as cholera
42
Q

How can lymphocytes recognise cells

A

The lymphocytes complementary to the antigens on self-cells will die or production will be suppressed. This is to prevent your lymphocytes from attacking your own cells.

This only remaining lymphocytes are complementary to pathogenic and non-self cells.
The same process occurs after birth in the bone marrow. Any new lymphocytes made in the bone marrow which are complementary in shape to antigens on self-cells will be destroyed.

43
Q

What causes symptoms of auto immune diseases

A

lymphocytes will attack self-cells are produced, this is what causes the symptoms of autoimmune diseases.

44
Q

What is an antigen

A

Antigens are molecules that generate an immune response by lymphocyte cells
when detected in the body.
They are usually proteins and they are located on the surface of cells.

45
Q

What is antigen variability

A

Pathogens DNA can mutate frequently. If a mutation occurs in the gene which codes for the antigen, then the shape of the antigen will change.
Any previous immunity to this pathogen (either naturally through prior infection or artificially through vaccination) is no longer effective, as all the memory cells in the blood will have a memory of the old antigen shape.
This is known as antigen variability. The influenza virus mutates and changes its antigens very quickly and this is why a new flu vaccine has to be created each year.

47
Q

Give two ways pathogens can cause disease

A

(Releases) toxins;
2. Kills cells / tissues.

48
Q

Putting bee honey on a cut kills bacteria. Honey contains a high concentration of
sugar.
Use your knowledge of water potential to suggest how putting honey on a cut kills
bacteria.

A

Water potential in (bacterial) cells higher (than in honey) / water
potential in honey lower (than in bacterial cells);

Water leaves bacteria / cells by osmosis;
(Loss of water) stops (metabolic) reactions.

49
Q

L enters the liver cells (lines 3−4).
Using your knowledge of the structure of the cell-surface membrane, suggest how
LDL enters the cell.

A

Lipid soluble / hydrophobic
2. Enters through (phospholipid) bilayer
OR
3. 4. (Protein part of) LDL attaches to receptor
Goes through carrier / channel protein.

50
Q

mutation of a tumour suppressor gene can result in the formation of a tumour.
Explain how.

A

umour suppressor) gene inactivated / not able to control / slow down
cell division;
2. Ignore: references to growth
Rate of cell division too fast / out of control

52
Q

Why does a person developed a large number of infections about 9 years after he first became
infected with HIV.

A

HIV destroys T cells;
More (free) viruses produced leads to fall in T-cells;
(So fewer) T-cells activate B-cells/memory cells;
Reduced/no antibody production;
Immune system not working properly/inability to fight infection;
Opportunistic infections;

53
Q

A test is carried out to see if a person is infected.
Explain why antibodies used must be monoclonal antibodies
And explain why that sepcific antigen binds to antibody

A

All have the same shape and only binds to the infection.

This is because they have a complimentary shape due to specific tertiary structure

54
Q

Destruction of phagocytes causes the lungs to be more susceptiblke to infections explain why

A

Phagocytes engluf/ingest pathogens/microogranisms bacteria and viruses.
They then destroy them
And lung diseases are caused by thes epathogens

55
Q

Phagocytes and lysosomes are involved in destroying microorganisms describe how

A

Phagocytes engulf pathogens / microorganisms;
Enclosed in a vacuole / vesicle / phagosome;
Lysosomes have enzymes;
That digest / hydrolyse molecules / proteins / lipids / microorganism;

56
Q

What is an antigen

A

Molecule / part of molecule / protein / glycoprotein / named molecule;
that stimulates an immune response / eq

57
Q

Describe how B-lymphocytes respond when they are stimulated by antigens.

A

Divide by mitosis / form clones; produce plasma cells;
(plasma cells)
make antibodies;
(plasma cells) produce memory cells;

59
Q

What is a vaccination eq

A

Injection of antigens / toxoids;
(Antigen from) attenuated microorganism / non-virulent
microorganisms / dead
microorganisms / isolated from microorganism;
Stimulates the formation of memory cells;

60
Q

Explain why there will be no colour change if mumps antibodies are not present in
the blood.

A

No antibodies to bind (to antigen);
Therefore 2 nd
antibody (with the enzyme) won’t bind / no enzyme /
enzyme-carrying antibody present
(after washing in step 4);

61
Q

What is an antibody

A

Protein / immunoglobulin;
specific to antigen;
idea of ‘fit’ / complementary shape;

62
Q

Describe how antibodies are produced in the body following a viral infection

A
  1. virus contains antigen;
  2. virus engulfed by phagocyte / macrophage;
  3. presents antigen to B-cell;
  4. memory cells / B-cell becomes activated;
  5. (divides to) form clones;
  6. by mitosis;
  7. plasma cells produce antibodies;
  8. antibodies specific to antigen;
  9. correct reference to T-cells / cytokine
63
Q

What is a monoclonal antibody

A

Reference to hybrid cell from tumour / cancer and
B-lymphocyte / hybridoma;
antibodies all the same / from one type of plasma cell;
specific to / complementary to / fits only one antigen;

64
Q

Explain why a test detects prostate cancer, but not any other disease.

A

Antibodies specific / only binds to PSA;
PSA only associated with prostate cancer / not with other
diseases;a

65
Q

Giv e two factors, other than cost, that should be considered when selecting an antibiotic to
treat a bacterial disease.

A

side effects / allergic reactions / low toxicity to cells;
interaction with other drugs / effective in conditions of use / reasonably stable;
should only act on the problem bacteria / narrow spectrum;
how much resistance the bacteria have built uo

66
Q

An antigen in a vaccine leads to the production of antibodies. Describe the part played by B
lymphocytes in this process.

A

Macrophages present antigens to B lymphocytes;
2 antigen binds to / is complementary to receptors on lymphocyte;
3 binds to a specific lymphocyte;
4 lymphocytes become competent / sensitised;
5 (B) lymphocytes reproduce by mitosis / (B) lymphocytes cloned;
6 plasma cells secrete antibodies;

67
Q

H epatitis B vaccine contains a viral antigen produced by genetically modified bacteria.
Describe how the isolated gene that codes for a protein in the virus’s coat could be
transferred to the bacterial cells.

A

Restriction enzyme / endonuclease;
2 to cut plasmid / to form sticky ends in plasmid;
3 (use) ligase(to join) gene to plasmid;
4 culture bacteria with (in medium containing) plasmids
5 to allow uptake of plasmids / transformation;
6 use of cold shock / chemical treatment (to enhance uptake) / heat
shock;

68
Q

Describe how T lymphocytes recognise and respond to the influenza virus.

A

T ymphocyte receptors recognise shape of haemagglutinin /
neuraminidase / viral antigen;
clone (once only);
destroy virus;

69
Q

D escribe how B lymphocytes respond to the influenza virus.

A

Clone (once only);
produce antibodies;
effect of antibody e.g. stimulation of phagocytosis /
precipitation of toxins;

70
Q

Describe the role of macrophages in stimulating B lymphocyte

A

Antigen in membrane presented to lymphocytes /
produce cytokinins;

71
Q

What is an attenuated microorganism

A

Microorganism alive/active;
But does not cause symptoms of disease/Avirulent;

72
Q

D escribe how HIV is replicated after it has entered a human cell.

A

Reverse transcriptase;
Accept integrase/description of action of
Enzyme uses (HIV) RNA to make DNA (copy);
DNA joined to (host) cell’s DNA/chromosome;
DNA used to make HIV RNA (copies);
Accept (HIV) DNA replicated when (T) cell divides
And HIV capsid proteins/enzymes;
Made at (host) ribosomes;
Assembly of new virus particles;
Budding off from membrane (of host cell);

73
Q

The destruction of T-cells by HIV leads to the death of an infected person.
Explain how.

A

Not enough/no T-cells to activate B-cells/lead to antibody production/
activate immune system;
Accept death of T-cells weakens the immune system
Person unable to fight /more prone to (opportunistic) infections/cancer;
Accept diseases
Example of infection/cancer;

74
Q

Describe how new viruses are produced after HIV has infected a T cel

A

DNA copy made (of viral RNA);
Inserted into host DNA / chromosomes;
(Uses viral DNA to) make viral proteins/particles;
Makes viral RNA;
(Host) cell makes new viruses;
“Budding off” / wrapped in cell membrane;

75
Q

Describe how humans produce antibodies against a pathogen such as Salmonella.

A

S almonella pathogen has specific antigen on surface;
Salmonella pathogen engulfed by macrophage;
T-cells activate B-cells;
B-cell with complementary/specific receptor antibody activated/
clonal selection;
B-cells divide/form clone/clonal expansion;
Plasma cells make antibodies;
Specific to antigen/bind to salmonella bacterial antigen;

76
Q

Why dont antibiotics work for viral infection

A

tibiotics stop metabolism, viruses don’t have metabolism;
Viruses hide in cells, antibiotics can’t reach;
Two suitable cell components antibiotics work against that
viruses don’t have;

77
Q

Give two ways in which pathogens can cause disease when they enter the body of their
hos

A

Da mage / destruction of cells / tissues;
Production of toxins;