Immunity Flashcards

(61 cards)

1
Q

Self

A

Your body recognises the antigens on your body as your own

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2
Q

Non self

A

Anything with different antigens to you stimulates an immune response

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3
Q

Antigens

A
  • on the surface of all cells are chemical markers called antigens.
  • each antigen has its own unique shape.
  • all cells have specific proteins on their surface membrane that identify it called antigens.
  • it is a protein found on the outside of cells, that triggers an immune response.

They enable the immune system to identify:
- pathogens (micro-organisms that cause disease)
- cells from other organisms of the same species (e.g. in transplanted organs)
- abnormal body cells (e.g. cancerous cells)
- toxins (poisonous molecules often released by bacteria)

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4
Q

What happens if you have an auto immune disease?

A

Your body starts attacking your own cells.

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5
Q

Phagocytes

A
  • made in the bone marrow, travel in capillaries but can squeeze through walls into tissues
  • 2 types; neutrophils and macrophages
  • ## patrol the body, searching for invadersPresent some of the pathogenic antigens on their own cell membrane
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6
Q

Neutrophils

A

Engulf and digest pathogens (and dead human cells/debris)

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7
Q

Macrophages

A

Can punch holes in the bacteria or stick proteins to the outside of the bacteria to make them more appealing for the neutrophils to destroy

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8
Q

Phagocytosis

A

Cellular process of engulfing solid particles using the cell membrane - carried out by phagocytes
Digests bacteria into soluble debris

1.Pathogen recognised as having foreign/non- self antigens. Pathogen attached
to phagocyte by antibody and surface receptors

  1. Pathogen is engulfed by phagocyte by
    endocytosis forming a phagosome.
  2. Lysosomes fuse to phagosome to
    form a phogolysosome and release H2O2,
    HCl, and digestive enzymes into phagosome to digest pathogen
  3. Harmless products removed (egested /
    excreted) by exocytosis or used by phagocyte
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9
Q

How do phagocytes detect invaders?

A
  • receptors on phagocytes recognises a non human cell and begins to engulf it
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10
Q

Endocytosis

A

Infolding of the membrane to create an internal vesicle

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11
Q

Phagosome

A

Name for vesicle containing pathogen

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12
Q

Lysosome

A

Contain h202 hydrochloric acid and digestive enzymes

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13
Q

What are people prescribed to help reduce the risk of rejection from a transplanted organ?

A

Immunosuppressants

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14
Q

Phagolysosme

A

Formation of phagocyte and lysosome
- the enzymes are breaking down the pathogen

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15
Q

Exotyosis

A

Releasing it out

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16
Q

Is phagocytosis a specific or non specific immune response? Why?

A

Non specific and it is not enough to cope with large numbers of pathogens e.g. flu virus

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17
Q

What is an APC

A

Antigen presenting cell

APCS activate T cells
APCs binding T helper cells, which stimulate and recruits more phagocytes and T cells to assist in the immune response.
This includes cytotoxic (killer) T cells which
destroy infected or foreign cells by releasing chemicals e.g perforin (makes pores in the membrane) into the invaded cell.

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18
Q

What are the two parts of specific immune responses

A
  1. Cell mediated response
  2. Humoral response
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19
Q

Cell mediated response

A

▪ APC’s can be either phagocytes or cells that have been invaded
▪ Once phagocytosis has taken place, pathogenic antigens are presented on the cell membrane
▪ T cells respond to the cell which is presenting the antigens
▪ T helper cells respond first – they have receptors which fit exactly to the presented antigens
▪ This activates the T cells and they begin to differentiate and recruit other T cells and activate B cells.

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20
Q

Roles of T cells

A
  1. T helper cells:
    a) Stimulate cytotoxic T cells to divide and proliferate
    b) Stimulate further phagocytosis
    c) Stimulate B cells to divide
    d) Develop into memory T cells for future infection
  2. Cytotoxic T Cells
    a) Seek out cells with foreign antigens (APCs)
    b) Attach to invaded cell and secrete toxic
    substances to kill it
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21
Q

Humeral response

A

Involves specialised white blood cells called b lymphocytes which target pathogens by producing antibodies

Activated T cells can then also activate B cells causing them to divide by mitosis, this is the start of the humoral response – we will look at this in more detail in the next lesson.

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22
Q

Immune response

A

Pathogen gets past chemical and physical barriers (skin/ stomach acid) and enters the blood then the white blood cells are the
second line of defence.

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23
Q

T cells

A

• T- cell (T-lymphocyte) another type of WBC.
• It has receptor proteins on its surface that bind to complementary antigens presented to it by phagocytes. This activates the T-cell
• Different types of T-cells respond in different ways.
• Helper T-cells
• Cytotoxic T-cells
• Helper T-cells also activate B-cells which secrete antibodies.

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24
Q

Humoral response - b cells and antibodies

A

• B lymphocytes (B cells) white blood cells involved in specific immune response
• B cells mature in bone marrow as well as being produced there

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25
B cells
• The B cells (B-lymphocytes) another type of WBC. Covered in antibodies- proteins which bind to antigens to form an antigen-antibody complex. • Each B-cell has a different shaped antibody on its membrane- so different ones bind to different antigens. • When an antibody on the surface of B-cell meets a complementary shaped antigen- it binds. This together with substances released from the helper-T cells, activates B-cell. • This is clonal selection. The activated B-cell divides into plasma cells. • The B-cells get the antigen from pathogens or APCs and presents the antigen on its cell surface membrane. • T helper cells bind to this antigen to active the B cells. • The B cells begin to divide by mitosis (clone themselves) to form plasma cells and memory cells this is known as clonal selection. • All B cells are now monoclonal antibodies • Plasma cells produce antibodies that are complimentary to the antigens. (primary response) • The memory cells stay in the blood stream circulating. If they come into contact with the antigen again they divide to form plasma cells and memory cells again. (secondary immune response)…
26
What is b cells activation
• Approx 10million different B cells- which have antibodies on their surface complementary to 10mill different antigens 1. Antigens in the blood collide with complementary antibody on a B cell. B cell takes in the antigen (endocytosis) and presents on the surface. 2. B cell then collides with helper T cell receptor- activates the B cell to go through clonal expansion and differentiation- clonal selection 3. B cells undergo mitosis-make large numbers of cells differentiate into plasma cells or memory B cells 4. Plasma cells = antibodies 5. memory B cells- divide rapidly into plasma cells therefore make large number of antibodies rapidly- 2nd infection response is faster and larger numbers
27
Memory b cells
• Memory B cells live for decades compared to plasma cells- short life cycle • Memory B cells do not make antibodies- divide by mitosis making plasma cells divide rapidly if they collide with a previously encountered antigen • Active Immunity- exposed to the pathogen- gained immunity
28
Antibodies
Antibodies are proteins which are specific to an antigen as they have a complementary shape. Antibodies can bind to antigens to form an antigen-antibody complex.
29
Structure of antibodies
- made of multiple amino acid chains (quaternary structure) connected by disulphide bridges - all antibodies have the same constant reagion that allow them to bind to receptors on immune system cells. - they have to variable regions which are the antigen binding sites
30
Antibodies work in 3 ways
Agglutination Neutralising toxins Preventing viruses from entering host cells
31
Agglutination
- antibodies cause microbes to clump together - makes it easier for phagocytes to engulf more of them at once
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Neutralise toxins
- some pathogens make us ill by producing toxins - some antibodies work by neutralising these toxins
33
Preventing viruses from entering host cells
- viruses have proteins on their surface which recognise and bind to receptors on the surface of the host cell - this is how many viruses enter their host cell - antibodies can bind to viruses and stop them attaching to their host cell
34
Anti genic variability
• Memory cells explains why we generally only catch chicken pox or measles once. The pathogens causing each of these diseases are of a single type and thus have the same antigen. • Some pathogens can form different strains (caused by mutations in genetic material) which often have different antigens – this is called antigenic variation. • This means that if you are re-infected a second time the memory cells will not recognise the antigen and won’t be activated and the antibodies made last time won’t be complimentary so the body has to start again with the primary response so you still get symptoms. • Antigenic variation is common in influenza and HIV, they make it hard to produce vaccines against these pathogens. • Every year a new flu vaccine has to be made that is most effective against the most recently circulating strain of the virus in the population. • We are seeing mutation in Covid-19 that has caused the new variant but at the moment there hasn’t been a significant mutation to the antigen to make the current vaccine not work.
35
Passive immunity
Artificial immunity input from us. - breast feeding - vaccine • The body is given the antibodies that have been made by a different organism. • Natural passive immunity – a baby gets antibodies through placenta and in breast milk • Artificial passive immunity - you are injected with antibodies e.g. if you get tetanus, you will be injected with antibodies against tetanus toxin. • Short term as no immune response involved and no memory cells produced
36
Natural immunity
Something your body does on it one - has no input from us • The body makes antibodies after being exposed to an antigen • Natural active immunity – you become immune after catching the disease. • Artificial active immunity- you become immune after being given a vaccination containing harmless dose of the antigen. • Long term protection because memory cells produced.
37
Problems with passive immunity
• Maternal antibodies pass placenta into foetal blood • Breast feeding passes antibodies present in the colostrum (first milk produced after giving birth) • Protection is temporary and only lasts few months after birth - Ab will be broken down in the spleen & liver, and no memory cells are formed
38
Vaccine
A way of introducing antigens of a dead or weakened pathogen into the body to stimulate the production of antibodies and memory cells. Vaccines are long lasting because they produce memory cells which can produce complimentary antibodies to the antigen in the future.
39
Preparing vaccines
Pathogens are made harmless by: • Killing but leaving antigens unaffected e.g. Cholera vaccine • Weakening (attenuation - heating) but leaving antigens unaffected e.g.oral vaccine against polio • Purified antigens removed from pathogen e.g. vaccine against hepatitis B • Using inactivated toxins called toxoids that are harmless but trigger same immune response e.g Tetanus injection
40
Why done vaccines eliminate all diseases?
Fails to induce immunity in some people (immunodeficiency) People get infected before enough antibodies are generated by vaccine to afford protection (slow primary response) Antigenic variability – pathogen mutates and vaccines no longer work Many different strains can’t all be fought at once Objections to vaccinations based on moral, religious and ethical grounds
41
Ethical issues with vaccines
• All vaccines are tested on animals first (same as all drugs) • Humans in clinical trials may put themselves at risk because they believe they may be “immune” • Some people refuse vaccines over fears of side effects, they are protected by herd immunity in the same way that people who can’t get the vaccine. • If there was a new disease, difficult decisions would be made about who would be the first to receive it → we are living this now!
42
Cholera
– Intestinal disease hard to reach by immune system – Symptoms of disease include chronic diarrhoea therefore oral treatments rapidly flushed out – High mutation rate leading to antigenic variability – Mobile populations increase the spread
43
Tuberculosis
– HIV increase led to many susceptible to TB – Overcrowding, poor accommodation in poverty / war-affected countries – Mobile populations – Growing elderly population who have less effective immune system resulting in susceptibility
44
Herd immunity
• ‘Herd immunity’ is a concept used for vaccination, in which a population can be protected from a certain virus if a threshold of vaccination is reached. • Herd immunity is achieved by vaccinating a large amount of the population so that enough people are immune to the virus it cannot spread far through the population. This protects those who cannot have the vaccine for medical reasons.
45
HIV structure
- has a spherical structure *contains a core of genetic material (RNA) and some proteins needed for viral replication *outer coating of protein - capsid * extra outer layer of protein - envelop * protruding from the envelop are lots of copies of an attachment protein that help HIV attach to the host helper T cell
46
What is HIV?
- human immunodeficiency viruses are two species of lentivirus that infect humans - HIV works by infecting helper T cells. The virus replicates in the T cells using their cellular machinery, eventually the cells swell and burst. - overtime, the number of T cells decreases and eventually causes acquired immunodeficiency syndrome (AIDS) - AIDs is a condition which is caused by failure of the immune system which allows opportunistic infections and cancers to thrive in the body - people with HIV are said to be HIV positive, they can be diagnosed through a low white blood cell count or through a test to check for presence of viral DNA.
47
How does HIV replicate?
1. Glycoprotein molecules on the virus surface bind to CD4 receptors on the surface of T helper cells. This allows the envelope surrounding the virus to fuse with the T helper cell membrane. 2. The capsid is released into the cell where it releases the RNA and reverse transcriptase. 3. Reverse transcriptase is used to make DNA from the HIV RNA template 4. The DNA is inserted into the cells DNA which gets replicated when cells replicate 5. DNA used to make HIV RNA and proteins at host ribosomes 6. Virus particles are assembled which bud off from the cells DNA membrane and go on to infect other cells - when leaving it ruptures the cell and dies. HIV attachment proteins are foreign antigens that can be recognised by the immune system - however - due to antigenic variation it helps HIV evade destruction from the immune system.
48
HIV’s impact on Host Cells
What happens? HIV infects and eventually kills helper T cells which act as host cells. Helper T cells are responsible for sending chemical signals that activate phagocytes, cytotoxic T - cells and B - cells - huge impact on immune response, therefore, the body can’t mount an effective response without the helper T - cells.
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Stages of infection
Initial infection - During intial infection period - HIV replicates rapidly and the infected person can experience severe flu like symptoms. After this, replication drops to a lower level - latency period During latency - the infected person won’t experience any symptoms Immune response will destroy some but not all the virus - small amounts mean and continue to replicate As HIV replicates and the amount of virus increases, therefore helper T - cell count drops which leads to AID’s.
50
Transmission of HIV
You can only be infected with HIV through another person with the virus. HIV is found in the blood and the sexual fluids of an infected person, and in the breast milk of an infected woman. - Having unprotected sex with an infected person Close contact with an infected persons blood e.g. sharing needles for drug use - Use of infected blood in a blood transfusion - Mother to child - a mother with HIV giving birth to a child or a child drinking the mothers milk - this is known as a vertical transmission Babies must be tested at 18 months as it takes time for the virus to replicate and be detectable.
51
Symptoms of AIDS-
- Lots of minor infections of mucosal membranes and recurring respiratory infections caused by a lower than normal number of helper T cells. - can take around 10 years for a HIV positive patient to develop the symptoms of AIDS. This is because the virus can remain dormant as DNA in host cells. - as AIDS progresses the number of immune system cells decreases further.
52
Treatment for AIDS -
- antiretroviral drugs are now available which after 6 moths can reduce the viral load in the body to an undetectable level - means patients can’t pass on HIV - pre exposure prophylaxis is an HIV prevention strategy - two people have been ‘cured’ of HIV using stem cell therapy where chemotherapy killed their white blood cells and they received a bone marrow transplant from someone with a naturally occurring CD4 mutation. However, too aggressive and expensive to be used as a regular HIV cure.
53
Monoclonal antibodies
Antibodies are produced by plasma cells which are all clones of one B cell hence the name monoclonal They are useful because they can be produced outside the body and they are reactive with only one type of antigen.
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Uses of monoclonal antibodies
Three main medical uses: -to target medication to specific cell types by attaching a therapeutic drug to an antibody - pregnancy testing - medical diagnosis by identifying proteins or antigen presence using the ELISA test
55
Radio immunotherapy
- links radioactive atoms to Monoclonal antibodies that deliver the radioactivity by being complimentary and only binding to antigens only found on cancer cells - doctors can concentrate radiation at tumour sites, reducing the amount of radiation that reaches healthy tissue - doctors can also use it to find tumours that may spread in the body to target therapy where it is needed.
56
Pregnancy testing
- antibodies complimentary to hCG protein are bound to a coloured bead - hCG in urine binds to antibodies - urine moves up the strip carrying beads - immobilised antibodies which bind to hCG create first ‘blue line’ - immobilised antibodies which bind to coloured beads create second ‘blue line’ if hCG is present
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What does ELISA stand for
Enzyme Linked ImmunoSorbent Assay
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ELISA Testing
Can be used for the presence of any antigen or antibody E.g. HIV diagnosis or allergies - an antibody is bound to an enzyme - the enzyme reacts with a substrate to produce a colour change - the antibody will be complementary and bind to the antigen or an antibody the test is designed to detect - there is a washing step which will remove any unbound antibodies so the more antigen there is in the sample the more colour change there will be because the more enzymes will be present to react with the substrate.
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ELISA tests - direct and indirect
Direct - this just involves one antibody binding to an antigen - used to look for the presence of an antigen in a sample Indirect - this uses multiple antibodies and can be used to look for antibodies that are complimentary to a specific antigen in a sample
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Indirect ELISA
- Antigens are immobilised and the sample being checked for antibodies is added. • If antibodies are present they will bind to the antigen. • A wash step occurs before the second antibody is added to remove any antibodies that are not bound to the antigen. • The second antibody has the enzyme attached which will cause the colour change and it is complimentary to the antibodies which would be attached the antigens. • A wash step occurs before the substrate is added to remove any antibodies that are not bound to the antibodies which are bound to the antigen • The substrate is added and if there are secondary antibodies present the enzyme they carry will cause the substrate to change colour. The darker the colour the more antibodies are present
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Efficiency of ELISA tests
• Indirect ELISAs can be more sensitive than direct detection methods, but there is also the risk of cross- reactivity with the antigen, which could cause higher background readings. • Indirect ELISAs also take longer due to the extra step. An advantage is that you can use the same secondary antibody (with the enzyme) for multiple different assays.