3.2.4 - cell recognition and the immune system Flashcards

(57 cards)

1
Q

what are non-specific defences?

A

the bodies defence mechanisms (physical or chemical barriers) which target all pathogens in the same way

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2
Q

non-specific defences - skin?

A

surface layer of dead cells - difficult to penetrate
surface covered with oily sebum - slightly acidic layer can prevent growth of harmful bacteria
healthy skin has harmless microorganisms which reduce pathogen growth by competing for resources
if there is a wound, blood clots to form a scab and stop pathogens getting in

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3
Q

non-specific defences - eyes?

A

eyelashes prevent things getting in
tears contain lysosomes

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4
Q

non-specific defences - nose?

A

contains mucus to trap pathogens
sneezing (expulsive reflex) expels pathogens

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5
Q

non-specific defences - mouth?

A

saliva contains lysosomes
coughing and vomiting (expulsive reflexes) expel pathogens
trachea has goblet cells which produce mucus to trap pathogens and cilia which beat to push mucus out of trachea

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6
Q

non-specific defences - stomach?

A

mucus contains hydrochloric acid which kills pathogens

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7
Q

what are phagocytes?

A

white blood cells which carry out phagocytosis (neutrophils and macrophages)

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8
Q

what is phagocytosis an example of?

A

a non-specific defence (phagocytes kill any pathogen)

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9
Q

what happens during the process of phagocytosis?

A
  1. the pathogen produces chemoattractants (toxins) which attract the phagocyte
  2. the phagocyte binds to receptors on the pathogen cell
  3. the phagocyte engulfs the pathogen by endocytosis, and the pathogen is contained in the cell within a phagosome
  4. lysosomes fuse with the phagosome, forming a phagolysosome
  5. the lysosomes release lysosymes into the phagolysosome, which hydrolyse the pathogen
  6. the products of hydrolysis are egested from the phagocyte by exocytosis
    specific to macrophages:
  7. the phagocyte presents the antigens from the pathogen on its surface, so it becomes an antigen presenting cell (APC)
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10
Q

what does each type of cell have on its surface?

A

specific molecules which identify it - these include proteins, and allow the immune system to identify pathogens, cells from other organisms of the same species, abnormal body cells and toxins

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11
Q

what are lymphocytes?

A

cells which are part of the specific response to antigens and are produced in the bone marrow

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12
Q

where does each type of lymphocyte mature?

A

B lymphocytes - bone marrow
T lymphocytes - thymus

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13
Q

what is the cell-mediated/cellular response?

A

the response of T lymphocytes to a foreign antigen

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14
Q

what happens during the cellular response?

A
  1. receptors on T cells (TCRs) bind to the antigens on antigen-presenting cells
  2. this activates the T cell which undergoes clonal expansion (mitosis to produce many genetically identical daughter cells)
  3. the cloned T cells differentiate into different specialised T cells (cytotoxic, memory, helper)
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15
Q

what are interleukins?

A

a type of cytokine which triggers an activated T helper cell to undergo mitosis (clonal expansion), and trigger macrophages to carry out phagocytosis

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16
Q

what is the role of helper T cells (TH)?

A

they stimulate cytotoxic T cells, phagocytes and B cells (which are stimulated to divide and secrete antibodies)

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17
Q

what is the role of cytotoxic T cells (TC)?

A

they kill abnormal cells and infected body cells by releasing proteins called perforins which create pores in the cell membrane so all substances can move into the cell, causing cell death

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18
Q

what is the role of T memory cells (TM)?

A

they enable a rapid response on reinfection of the same pathogen

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19
Q

what is the humoral response?

A

the response of B lymphocytes to a foreign antigen

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20
Q

what do B cells have on their cell-surface membrane?

A

antigen receptors in the form of membrane-bound antibodies (IgM) - antibodies on different B cells bind to different antigens

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21
Q

what happens during the humoral response?

A
  1. a B lymphocyte encounters a pathogen with the correct antigen for its antibodies to bind to
  2. the B lymphocyte attaches to and engulfs the pathogen
  3. the pathogen is digested and the antigens are presented on the surface on the B lymphocyte (APC)
  4. an activated T helped cell uses its TCR to attach to the antigen on the B lymphocyte (clonal selection)
  5. the T helper cell produces interleukins which activate the B lymphocyte
  6. the B lymphocyte undergoes mitosis producing clones of plasma cells and memory cells (clonal expansion)
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22
Q

what is the role of the cloned plasma cells in the humoral response?

A

they release identical antibodies which bind to the antigens on the pathogen’s surface - disables pathogen, marks for phagocytosis or triggers agglutination (primary immune response)

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23
Q

what is the role of the cloned b memory cells in the humoral response?

A

they remain in the blood in case of reinfection with the same pathogen - if this happens, they turn into plasma cells and release antibodies (secondary immune response)

24
Q

what is an antibody?

A

a glycoprotein which is specific to an antigen as it has a complementary shape and binds to the antigen forming an antigen-antibody complex

25
what is the structure of an antibody?
they have 4 polypeptide chains (two long heavy, two short light) chains are held together by disulfide bridges they have 2 antigen binding sites they have a variable and a constant region
26
what is the variable region of an antibody?
the area at the end of antibodies which is different for each one
27
what is the constant region of an antibody?
the area which is the same for all antibodies (allows them to bind to the membrane on B cells)
28
what does the flexible hinge region on an antibody allow?
the distance between the antigen binding sites to vary
29
what does the formation of an antigen-antibody complex do?
lead to the destruction of the antigen
30
how do antibodies work?
1. bind to antigens or bacterial toxins to neutralise them 2. bind to viruses so they can't invade host cells (competitive inhibitor) 3. stick pathogens together so they can't infect cells (agglutination) 4. put opsonins onto cells they bind to which marks them for phagocytosis (opsonisation)
31
how is the secondary immune response different to the primary immune response?
it is faster and produces a greater number of antibodies
32
what are the possible contents of a vaccine?
1. attenuated pathogen 2. dead pathogen 3. toxoid (harmless toxin) 4. surface antigens
33
what are the features of an attenuated vaccine?
produces strong, long-lasting immune response unsuitable for those with weak immune systems as it can cause infection
34
what are the features of a dead vaccine?
suitable for those with weak immune system as can't cause infection doesn't trigger strong or long-lasting immune response - may require repeated doses or booster
35
what is natural immunity?
immunity stimulated by the infection of a pathogen
36
what is artificial immunity?
immunity stimulated as a response to a vaccine
37
what is active immunity?
production of antibodies by the body
38
what is passive immunity?
introducing antibodies from an external source
39
what is an example of natural, passive immunity?
antibodies passed from a mother to a baby via breast milk or the placenta
40
what are two ways that antigens try to hide from the body's immune cells?
1. antigenic variation - pathogen alters surface antigen so it can repeatedly infect host 2. antigenic concealment - pathogen hides antigens eg. lives inside cells, coats membrane in host proteins, remains in parts of body which are hard for vaccines to reach
41
what are vaccines used for?
to provide protection for individuals and populations against disease
42
what is herd immunity?
when as much of a population are vaccinated as possible to reduce potential transmission of disease
43
what is ring immunity?
vaccinating the group of people around someone infected with a pathogen, to prevent its transmission outside that community
44
how is HIV transmitted?
intimate human contact or direct exchange of bodily fluids eg. sexual intercourse, sharing of needles by intravenous drug users, mother to child across placenta, breast milk or through mixing of blood during birth
45
what are the key structural features of HIV?
genetic material - two RNA strands reverse transcriptase - uses viral RNA as a template to form viral DNA protein capsid - surrounds RNA and reverse transcriptase lipid envelope - formed from cell membrane of host T helper cell attachment proteins - gp 41 and gp 120
46
what is the process of HIV replicating in helper T cells?
1. using glycoprotein gp 120, HIV binds to CD4 receptor on helper T cell 2. capsid is injected into T helper cells 3. capsid partially dissolves (uncoating) so viral RNA and reverse transcriptase can be released 4. reverse transcriptase catalyses reverse transcription (single-stranded RNA into double-stranded DNA) using DNA nucleotides in cytoplasm 5. newly synthesised viral DNA is transported across nuclear membrane into nucleus 6. integrase catalyses integration of viral DNA into genome of host cell 7. genes in HIV DNA expressed in DNA of t helper cells - HIV proteins synthesised and new HIV RNA made 9. new HIV viruses released and T helper cell dies
47
how does HIV cause the symptoms of AIDS?
it kills helper T cells, meaning antibody production by B lymphocytes and the cell-mediated response are less effective this makes the individual more susceptible to opportunistic infections eg. tuberculosis, cancer
48
why can't antibiotics be used to treat viruses like HIV?
they kill bacteria by targeting bacterial cell structures or metabolic processes in bacterial cells however, viruses don't have a cellular structure, and they use the metabolic processes of the host cell
49
what is the ELISA test?
Enzyme-Linked Immunosorbent Assay test - allows you to determine the quantity of a protein
50
how is an indirect ELISA test conducted?
1. antigen molecules stick to the bottom of the well 2. the well is washed thoroughly to remove antigen molecules which didn't stick 3. an antibody specific to the antigen is added - the antibody molecules bind to the antigens 4. the well is washed again to remove excess antibody molecules 5. a secondary antibody is added which specifically binds to the first antibody, and is attached to an enzyme molecule 6. once the antibodies have bound, the well is washed again to remove excess secondary antibody 7. the substrate (normally colourless) for the enzyme is added, and the enzyme converts it into a coloured product molecule
51
what does the intensity of the colour produced in the ELISA test depend on?
the number of enzyme molecules, and therefore the number of antigen molecules present
52
how is the direct ELISA test different to the indirect test?
the antigen is also on the surface of the well, but no secondary antibody is added - the enzyme is bound to the primary antibody
53
how is a sandwich ELISA test conducted?
1. the antibody sticks to the bottom of the well 2. specific antigens are added and bind to the antibody 3. an antibody which is complementary to that antigen-antibody complex and has an enzyme attached is added and binds 4. the substrate for the enzyme is added and the colour change occurs
54
what are monoclonal antibodies?
a single type of antibody which can be isolated and cloned
55
how can monoclonal antibodies be used in targeting medication?
1. direct - monoclonal antibodies can be designed with a binding site complementary to the antigens on the outside of cancer cells, and while these antibodies are bound to the antigens, it stops the chemicals which enable uncontrolled cell division from binding, so the cancer cells don't grow 2. indirect - monoclonal antibodies with binding sites complementary to the antigens on cancer cells can have drugs attached to them which are delivered directly to the cancer cells and kill them
56
how can monoclonal antibodies be used in medical diagnosis?
in the ELISA test they can diagnose pregnancy, hepatitis, flu, chlamydia, prostate cancer etc.
57
what ethical issues are associated with using monoclonal antibodies?
mice are used to produce the antibodies initially and they die as their spleen must be removed - this raises questions about whether using animals like this is justified as it does better treatment and detection of disease there are dangers with testing the safety of some monoclonal antibodies - there have been cases where they have been tested on human volunteers who then suffered multiple organ failure