Topic 2.4 - The Immune System (F) Flashcards

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1
Q

What are the general causes of disease? (3)

A

Lifestyle (e.g. smoking, alcohol, no exercise)
Genetic defect - caused by a mutation in the DNA coding for a protein
Infection - caused by a pathogen : a microbe (bacteria fungus, virus or protocista) that causes illness

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2
Q

How do pathogens cause disease

A

-Damage host tissues by breaking cell membranes or preventing DNA, RNA and protein synthesis
-Produce toxins

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3
Q

What is an antigen

A

-An antigen is any part of an organism or substance that the immune system recognises as foreign.
-Cell-surface molecule which stimulate immune response. Usually (glyco)protein, sometimes (glyco)lipid or
polysaccharide.
-Immune system recognises as “self’ or “non-self’ = enables identification of cells from other organisms of same species, pathogens, toxins & abnormal body cells.

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4
Q

What role does the lymphatic vessels have in the immune system

A

-They contain lymphatic fluid that circulates and removes waste and harmful substances from the body

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5
Q

What role do lymph nodes have in the immune system

A

-Filters that remove harmful substances. They contain white blood cells called lymphocytes.

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6
Q

What is the 1st line of defence in immunity (outline)

A

Skin creates a barrier to infection

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7
Q

What is the 2nd line of defence in immunity (outline)

A

White blood cells respond non-specifically

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8
Q

What is the third line of defence in immunity

A

Specific responses from lymphocytes

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9
Q

What is a non-specific immune response and give examples

A

Response is immediate and always the same (e.g. phagocytosis and physical barriers)

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10
Q

What is a specific immune response and give examples

A

Response is slower and different for each pathogen (e.g. cell-mediated and humoral)

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11
Q

Give two differences between non-specific and specific immune responses

A

Non-Specific = same for all pathogens
Specific = has a complementary pathogen

Non-Specific = immediate
Specific = time lag

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12
Q

What are some physical barriers in the first line of defence

A

-Tears contain lysosome
-Stomach acid and enzymes kill bacteria.
-Epithelial layer of the skin is tough and consists of keratin
-Cilia and mucus lining respiratory surfaces
-Platelets > damaged skin (blood clots)
-Gut and skin flora competes with pathogens for food and space

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13
Q

What is the second line of defence : phagocytosis (in depth)

A
  1. The phagocyte is attracted to the pathogen by chemicals produced by pathogens (chemotaxis)
  2. The phagocyte binds to the pathogen and engulfs it via endocytosis forming a phagosome
  3. Lysosomes migrate towards the phagosome
  4. The lysosomes release their lytic enzymes into the phagosome where the pathogen is broken down
  5. Phagocyte absorbs the products from pathogen hydrolysis
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14
Q

What happens to the breakdown products of a pathogen after phagocytosis

A

They are absorbed by the phagocyte and presented on their cell membrane

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15
Q

Brief overview of B-lymphocytes

A

-Involves B lymphocytes (B-cells)
-Made and develop in the bone marrow
-Found in body fluids (e.g. blood, lymph and plasma)
-Make antibodies
-Respond to foreign bacteria and viruses

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16
Q

Outline the process of humoral response (B-Cells)

A
  1. After phagocytosis some antigens from the pathogen are displayed in the phagocytes surface (antigen presentation.)
  2. T-Helper cells attach to the antigens and stimulate complementary B-Cells through releasing cytokines to divide by mitosis
  3. The cloned B-Cells develop and differentiate into plasma and memory cells
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17
Q

Outline primary immune response (humoral)

A
  1. The cloned B-lymphocytes develop into plasma cells which secrete antibodies directly and destroy the pathogen and any toxins
  2. They only live a few days and secrete 2000 antibodies per second.
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18
Q

Outline secondary immune response (humoral)

A
  1. The cloned B-lymphocytes develop into memory cells which do not secrete antibodies
  2. They circulate in the blood and tissue fluid and divide rapidly into more plasma cells and memory cells when they encounter the same pathogen again,
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19
Q

Brief overview of T-lymphocytes

A

-Made in the bone marrow but mature in the Thymus
-Respond to bodies own cells altered by cancer, cells infected with viruses and to transplanted tissues

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20
Q

Outline the process of cell-mediated response (T-Cells)

A

-Abnormal or transplanted cell or antigen presenting phagocyte
-T-Helper cell with complementary receptor bind to the antigen
-They then differentiate into different types of T-Cells through release of cytokines which stimulate rapid mitosis

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21
Q

Outline the different types of T-Cells that they differentiate into during cell-mediate immune responses

A

-TC cells (cytotoxic T cells) : kill virus infected cells or cancerous cells by making holes in their membranes
-TH cells (helper T cells) : Stimulate (humoral immunity) B-lymphocytes to divide or become memory cells

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22
Q

Explain the role of Antigen-presenting cells (APCs)

A

-Phagocytes with presenting antigens from pathogen on surface (after hydrolysis in phagocytosis)
-Enhances recognition by T-helper cells, which cannot directly interface with pathogens/antigens in body fluid

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23
Q

Outline memory cells response to antigens

A

They respond to specific antigens on the surface of pathogens and on a second encounter it is easily identified and destroyed

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24
Q

Outline how monoclonal antibodies are made

A

Plasma cells are indentical to the B-cell and they secrete loads of antibodies specific to the antigen. (Monoclonal antibodies)

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25
Q

Outline how monoclonal antibodies work

A

-They bind to the antigens on the surface of the pathogen to form lots of antigen-antibody complexes.

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26
Q

What is agglutination

A

-An antibody has two binding sites so binds to two pathogens at the same time so they become clumped together.
-Phagocytes then bind to the antibodies and phagocytose many pathogens are once destroying the pathogens

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27
Q

Structure of an antibody

A

-They are proteins so made up of chains of amino acids.
-The specificity depends on the variable regions which form the antigen binding sites, each variable region has a unique tertiary structure that’s complementary to one specific antigen
-All antibodies have the same constant regions

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28
Q

The primary response

A

-When an antigen enters the body for the first time the response is slow as there aren’t many B-Cells which can make the antibody needed to bind to it. Eventually the body will produce enough to overcome the infection, but will be showing symptoms.
-Both T and B-cells produce memory cells which remain in the body for a long time. Memory T-Cells remember the specific antigen and memory B-Cells record the specific antibodies needed to bind the antigen. The person is now immune.

29
Q

The secondary response

A

-If the same pathogen enters the body again, the immune system will produce a quicker stronger response
-Memory B-Cells are activated and divided into plasma cells that produce the right antibody to the antigen. Memory T-Cells are activated and divided into the type of T-Cells to kill the cells carrying the antigen. The secondary response often gets rid of the pathogen before symptoms show.

30
Q

What is active immunity

A

The type of immunity when your immune system makes its own antibodies after being stimulated by an antigen.

31
Q

What are the two types of active immunity

A

Natural - when you become immune after catching a disease
Artificial - When you become immune after given a vaccination containing a harmless dose of antigen

32
Q

What is passive immunity

A

You get from being given antibodies made by a different organism - your immune system doesn’t produce any antibodies of its own

33
Q

What are the two types of passive immunity

A

Natural - This is when a baby becomes immune due the antibodies it receives from its mother through the placenta and in breast milk
Artificial - When you become immune after being injected with antibodies from someone else (e.g. tetanus can be injected with antibodies against tetanus toxin collected from blood donations)

34
Q

Compare active and passive immunity

A

-Active requires exposure to antigen whereas passive doesn’t
-Active takes a while for protection to develop whereas passive is immediate
-In active memory cells are produced but they aren’t in passive
-In active protection is long term as the antibody is produced in response to antigen presence whereas passive is short term as antibodies given are broken down.

35
Q

Outline active immunity vaccines

A

Injected and the bodies immune system is triggered, this provides long lasting protection against the pathogen

36
Q

Outline passive immunity vaccines

A

Antibodies are injected from an outside source, this is short acting.

37
Q

Outline how vaccinations work

A

Harmless dilute or heat attenuated pathogens contain antigens that cause the body to produce memory cells against a particular pathogen, without the pathogen causing disease. This means immunity without getting any symptoms

38
Q

What is herd immunity

A

-Vaccines protect individuals that have them and as they reduce the occurrence of the disease, those not vaccinated are also less likely to catch the disease.

39
Q

How are vaccines taken and what are the advantages/disadvantages of this

A

-Injected or orally taken
-If orally taken it could be broken down by enzymes in the gut or may be too large to be absorbed into the blood.
-Sometimes booster vaccines are given later on to ensure memory cells are produced

40
Q

What should vaccines be to be successful?

A

-Economical so vulnerable groups can be vaccinated
-Few side effects so people will be inclined to be vaccinated
-Mean if producing, storing and transporting the vaccine in hygienic and cold conditions
-Trained staff to administer the vaccines
-Must be able to vaccinate all vulnerable groups at one time to prevent transmission of the pathogen (herd immunity)

41
Q

Outline vaccine ethics in relevance to animals

A

-All vaccines are tested on animals before humans and some people disagree with this
-Animal based substances may be used to produce a vaccine

42
Q

Outline ethics of vaccines in relevance to testing

A

-Testing on humans can be risky (e.g. volunteers at risk of contracting disease as they think they’re fully protected such as unprotected sex after getting HIV vaccine which might not work)

43
Q

What are other ethical issues with vaccinations

A

-Some don’t want to take the vaccine due to the risk of side effects, but they are still protected because of herd immunity and others think this is unfair
-If there was an epidemic of a new disease there would be rush to receive it and difficult decisions would be made about who would be the first to receive it

44
Q

What is antigenic variability

A

-Memory cells respond to specific antigens on the surface to pathogens so it is easily identified and destroyed on a second encounter
-Some pathogens have antigens on their cells keep changing making them unrecognisable to existing memory cells.
-The immune response has to then carry out another primary response which takes take and therefore symptoms are present

45
Q

How does antigenic variability affect the development of vaccines (e.g. of flu:

A

-Makes it difficult
-Flu vaccine changes every year as the antigens on the surface of the influenza virus change regularly, forming new strains of the virus. Memory cells from vaccines will not recognise other strains with different antigens.

46
Q

What are monoclonal antibodies

A

-Antibodies produced from a single group of genetically identical B-Cells. This means that they’re all identical in structure.
-They can bind to anything specific you want (e.g. specific antigen) and will only bind to and target this molecule which can be useful for treating illness and in medical diagnosis

47
Q

How are monoclonal antibodies used as anti-cancer drugs

A

-Different cells in the body have different surface antigens. Cancer cells have antigens called tumour markers that are not found on normal body cells. Monoclonal antibodies can be made that will bind to tumour markers.
-You can also attach anti-cancer drugs to the antibodies and when they come into contact with the cancer cells they will bind to the tumour markers so the drug will only accumulate in the body where there are cancer cells. So, the side effects are lower than other drugs.

48
Q

How are monoclonal antibodies used as pregnancy tests

A

-They detect the hormone human chorionic gonadotropin (hCG) that’s found in urine of pregnant women
-The application area contains antibodies that are complementary to the hCG protein, bound to a colour bead
-When urine is applied any hCG will bind to the antibody on the beads, forming an antigen-antibody complex
-The urine moves up the stick to the test strip, carrying any beads with it
-The test strip contains antibodies to hCG that are stuck in place
If there is hCG present the strip turns blue as the antibody bind to hCG- concentrating the hCG-antibody consoles with the blue beads attached and if none i present no binding will occur so it won’t turn blue

49
Q

What is the ELISA test

A

Allows you to see if a patient has any antibodies to a certain antigen or any antigen to a certain antibody. It can be used in diagnosis to test for pathogenic infections (e,g, HIV), for allergies.

50
Q

How does the ELISA test work

A

An antibody is used which has an enzyme attached to it. The enzyme can react with a substrate to produce a coloured product causing the solution in the reaction vessel to change colour. If there’s a colour change it demonstrates that the antigen or antibody of interest is present in the sample being tested. In some types the quantity can be worked out by intensity of colour change

51
Q

Outline the direct ELISA test

A

-Uses a single antibody complementary to the antigen testing for
-Antigens from a patient sample are bound to the insid of a well in a plate and a detecting antibody that is complementary is added
-If the antigen is present it will be immobilised on the inside surface of the well and the antibody will bind to it.
-The well is was he out to remove unbound antibodies and a substrate solution is added and if the antibody is present the enzyme reacts to give a colour change giving a positive result

52
Q

Outline how indirect ELISA tests work

A

-Uses two different antibodies (e.g. HIV)
1. HIV antigen binds to bottom of well in well plate
2. Sample of patients blood plasma may contain different antibodies is added. If any specific HIV antibodies in the plasma they will stick to the antigen. The well is washed out to remove unbound antibodies
3. A secondary antibody that has a specific enzyme attached to it is added to the well. This secondary antibody can bind to the HIV antibody. The well is washed again and if there’s no primary antibody all of the secondary antibody will be washed away as there’s nothing to bind to
4. A solution which contains a substrate that reacts with the enzyme attached to the secondary antibody and produces a colour product is added. If the solution changes colour it indicates the patient has HIV antibodies in their blood and is infected

53
Q

What are ethical issues surrounding the use of monoclonal antibodies

A

-Involve animal rights as animals are used to produce the cells from which the monoclonal antibodies are produced. Some disagree with the use of animals in this way.

54
Q

What are HIV and AIDS

A

Human Immunodeficiency Virus affects the human immune system which eventually leads to acquired immune deficiency syndrome which is a condition where the immune system deteriorates and eventually fails which makes people more vulnerable to other infections like pneumonia

55
Q

Outline the initial infection of HIV

A

-Can enter the body via infected fluids; during sex, drug-taking through needles, blood infection, transfusions and potentially from mother to child across placenta via breast milk
-During the initial infection HIV replicates rapidly and the infected person may experience flu-like symptoms. After this period HIV replication drops - the latency period. During this period which can last for years the infected person won’t experience any symptoms.

56
Q

What is the process of HIV infection

A
  1. p120 molecules on HIV bind to CD4 receptor proteins on T-helper lymphocytes and macrophages
  2. The virus outer envelope fuses with the cell membrane
  3. Viral RNA and enzymes from the HIV are injected into the T-Cell
  4. The viral DNA is transcribed and translated by the host cell to produce new viral proteins
  5. Transcribed RNA plus viral proteins are assembled together to form new viruses
  6. The new viruses leave the cell by budding, taking some of the host cell membrane to form the viral envelope which kills the T-helper cells.
57
Q

Outline HIV Stage 1: Acute HIV syndrome

A

-After 3-12 weeks HIV antibodies found in the blood
-Person may experience symptoms of an infection (fever and swollen glands)
-Loss of T-Helper cells
-Infected T-Helpers are killed by T-Killers - reduces virus replication rate but doesn’t stop it

58
Q

Outline HIV Stage 2 : The Chronic Phase

A

-All symptoms disappear as T-Killer cells kill off infected CD4 T-Helper cells
-Can last for many years in fit healthy people
-Gradual tendency for disease susceptibility increases

59
Q

Outline HIV Stage 3: The disease stage

A

-Viral load becomes so great and the T-Helper level falls to below half its normal level
-Patients suffer AIDS-related symptoms such as fatigue, weight loss etc.

60
Q

Outline HIV Stage 4 : Advanced AIDS

A

-Immune system is so low that “opportunistic infections” can take hold.
-Patients can develop purple/black patches
-Significant weight loss
-Dementia can develop AIDS

61
Q

What are HIV symptoms

A

-Neurological: meningitis and encephalitis
-Eyes: Retinitis
-Lungs: TB, tumours and pneumonia
-Skin: Tumours
-Diarrhoea

62
Q

What are the symptoms of AIDS

A

-Minor infections of mucus membranes
-Number of immune system cells decreases furthers. Patients becomes susceptible to more serious infections
-During late stages low number of immune system cells and range of serious infections can develop which can kill the patient

63
Q

Outline HIV virus structure

A

-Spherical
-Core of RNA and some proteins (enzyme reverse transcriptase which is needed for virus replication)
-Outer coating of a capsid and then lined with membrane stolen from host cell which has attached proteins to attach to host helper T-Cell

64
Q

Outline process of HIV replication

A
  1. Attachment protein attach to receptor molecule on the cell membrane of host heller T-Cell
  2. Capsid is released into cell and releases RNA into the cells cytoplasm
  3. Inside reverse transcriptase makes complementary DNA strand from viral RNA template
  4. Double-stranded DNA is made and inserted into human DNA
  5. Host cell enzymes make viral proteins from viral DNA in host DNA
  6. The viral proteins are assembled into new viruses which bud from the cell and infect other cells
65
Q

Outline how antibiotics kill bacteria

A

-Interfere with their metabolic reactions by targeting the bacterial enzymes and ribosomes used in these reactions. Bacterial enzymes are specifically targeted so human cells aren’t damaged.

66
Q

How do antibiotics affect viruses

A

Viruses don’t have their own enzymes and ribosomes they use the host cells’. So antibiotics can’t inhibit viruses.

67
Q

How do antiviral drugs affect viruses

A

They are designed to attack the few virus-specific enzymes that exist

68
Q

How can HIV be controlled

A

-There in no cure, but antiviral drugs can slow down the progression in an infected person.
-Protection before infection is best way to control