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A LEVEL BIO > topic 2B - immunity > Flashcards

topic 2B - immunity Flashcards

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1
Q

examples of our bodies defence mechanisms against pathogens:

A

-physical and chemical defences
-inflammation
-recognising ‘foreign’ cells

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2
Q

examples of physical defence mechanisms against pathogens:

A

-skin
-mucus membranes
-tears (containing the enzyme lysozyme, which destroys bacteria)
-saliva

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3
Q

what is non-specific inflammatory response?

A

swelling and heating of the region invaded by the pathogen

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4
Q

what is a specific immune response?

A

recognising foreign cells and targeting any pathogenic cells

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5
Q

how is the body able to recognise foreign cells?

A

due to specific molecules found on the surface of cells

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6
Q

examples of molecules that help us recognise foreign cells:

A

-glycoproteins
-glycolipids

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7
Q

what do glycoproteins & glycolipids allow the body to recognise?

A

its own cells (‘self’) and foreign cells (‘non-self’):

-pathogens
-cells from other organisms of the same species
-abnormal body cells (cancerous)
-toxins

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8
Q

define antigens

A

markers that allow cell-to-cell recognition

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9
Q

self antigens

A

antigens produced by the organism’s own body cells

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10
Q

do self antigens stimulate an immune response?

A

no

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11
Q

which cells stimulate an immune response?

A

non-self antigens

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12
Q

what is antigen variability?

A

the antigens present on their surface change frequently due to genetic mutations

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13
Q

why is antigenic variability bad for mammals?

A

-lymphocytes and memory cells produce a specific immune response
-the surface receptors on lymphocytes and memory cells are complementary to only one antigen
-when the antigen on a pathogen changes the lymphocytes and memory cells can no longer bind, there is no secondary immune response
-the host gets infected and suffers from the disease again

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14
Q

what are phagocytes?

A

-white blood cells that are produced continuously in the bone marrow
-they are stored in the bone marrow before being distributed around the body in the blood

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15
Q

function of phagocytosis:

A

-removing dead cells and invasive microorganisms
-non-specific immune response

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16
Q

what are the two main phagocytes?

A

-neutrophils
-macrophages

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17
Q

define phagocytosis (simple)

A

the phagocyte engulfs the pathogen
the phagocyte forms a phagosome around the pathogen
the phagocyte releases lysosomes (contain hydrolytic enzymes) which digest the pathogen and destroy it
the pathogen is released

the process of recognising and engulfing a pathogen

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18
Q

what do all phagocytes carry out?

A

phagocytosis

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19
Q

neutrophil: key facts

A

-travel throughout the body and often leave the blood by squeezing through capillary walls to ‘patrol’ the body tissues
-during an infection, they are released in large numbers from their stores
-short-lived cells

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20
Q

how phagocytosis occurs with neutrophils

A

ENDOCYTOSIS:
1) chemicals released by pathogens, attract neutrophils to the site where the pathogens are located (chemotaxis)

2) neutrophils move towards pathogens and attach to them

3) once attached to a pathogen, the neutrophil engulfs it and trapping the pathogen within a phagosome

4) a lysosome fuses with the membrane of the phagosome (to form a phagolysosome) and releases lysozymes to digest the pathogen

5) the lysozymes destroy the pathogen

6) after killing and digesting the pathogens, the neutrophils die

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21
Q

what are lysosomes?

A

membrane organelles that contain digestive enzymes (lysozymes)

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22
Q

what is a sign of dead neutrophils?

A

pus

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23
Q

macrophages: key facts

A

-larger than neutrophils
-long-lived cells
-after being produced in the bone marrow, macrophages travel in the blood as monocytes, then they develop into macrophages once they leave the blood & settle in organs

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24
Q

how phagocytosis occurs with macrophages

A

-they cut the pathogens up so that they can display the antigens of the pathogens on their surface
-the cell is now an antigen-presenting cell & can then be recognised by lymphocytes

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25
Q

what are lymphocytes a type of?

A

white blood cell

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26
Q

what do lymphocytes play an important part in?

A

the specific immune response

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27
Q

what size are lymphocytes compared to phagocytes?

A

smaller than phagocytes

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28
Q

what fills most of a lymphocyte cell?

A

a large nucleus

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29
Q

where are lymphocytes produced?

A

in the bone marrow before birth

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30
Q

what are the two types of lymphocytes?

A

t-lymphocytes (t cells)
b-lymphocytes (b cells)

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31
Q

what happens during the maturation of T lymphocytes: steps

A

1) immature t-lymphocytes leave the bone marrow to mature in the thymus after they have divided

2) mature t-lymphocytes have specific cell surface receptors called t-cell receptors

3) these receptors have a similar structure to antibodies and are each specific to one antigen

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32
Q

when are t lymphocytes activated?

A

when they encounter (and bind to) their specific antigen that is being presented by one of the host’s cells (eg: macrophage or a body cell that has been invaded by a pathogen)

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33
Q

what are the two types of t cell?

A

-helper t cells
-cytotoxic t cells (killer t cells)

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34
Q

when will t cells bind to an antigen?

A

if it is present on the surface of an antigen-presenting cell

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35
Q

what is an antigen presenting cell?

A

one of the host’s cells that has been invaded by a pathogen and is displaying the antigen on its cell surface membrane

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36
Q

how do t-lymphocytes increase in number?

A

they divide by mitosis

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37
Q

what do t-helper cells do?

A

assist other white blood cells in the immune response

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38
Q

what do t-helper release & what is the effect of the released products?

A

they release cytokines (hormone-like signals) which stimulate:

-the maturation of B-lymphocytes into plasma cells
-the production of memory b cells
-the activation of cytotoxic t cells

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39
Q

where do b cells stay while immature and move when mature?

A

b-lymphocytes remain in the bone marrow until they are mature and then spread through the body, concentrating in lymph nodes and the spleen

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40
Q

how many b cells are produced throughout life and why?

A

-millions of types of B-lymphocyte cells are produced within us
-as they mature, the genes coding for antibodies are changed to code for different antibodies
-once mature, each type of B-lymphocyte cell can make one type of antibody molecule

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41
Q

b lymphocytes and antigens

A

part of each antibody molecule forms a glycoprotein receptor that can combine specifically with one type of antigen

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42
Q

define clonal selection

A

when an antigen enters the body for the first time, the small numbers of b-lymphocytes with receptors complementary to that antigen are stimulated to divide by mitosis

OR

the process of matching the antigens on an APC with the antigen receptors on B and T lymphocytes

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43
Q

define clonal expansion

A

cell division of the activated B or T lymphocyte after clonal selection

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44
Q

which two cells do b cells divide into?

A

-plasma cells
-memory cells

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45
Q

what do plasma cells do?

A

secrete lots of antibody molecules (specific to the antigen)

into the blood, lymph or linings of the lungs/gut

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46
Q

lives of plasma cells

A

-short-lived (their numbers drop off after several weeks)
-the antibodies they have secreted stay in the blood for a longer time

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47
Q

what do b cells remaining in the blood become?

A

memory cells

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48
Q

what are antibodies?

A

proteins that bind to antigens as a part of the immune response

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49
Q

what structure do antibodies have?

A

a quaternary structure (which is represented as Y-shape)

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50
Q

components of antibodies

A

-two ‘heavy’ polypeptide chains bonded by disulfide bonds to two ‘light’ polypeptide chains
-constant region
-variable region

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51
Q

the variable region of an antibody

A

-different for each antibody.
-where the antibody attaches to the antigen to form an antigen-antibody complex

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52
Q

what is at the end of the variable region of an antibody?

A

the antigen-binding site (composed of 110 to 130 amino acids)

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53
Q

why do the antigen-binding sites vary greatly?

A

to give the antibody its specificity for binding to antigens, the sites are specific to the epitope

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54
Q

what is the epitope?

A

the part of the antigen that binds to the antibody

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55
Q

what is the hinge region of an antibody and what does it do?

A

-where the disulfide bonds join the heavy chains)
-gives flexibility to the antibody molecule -allows the antigen-binding site to be placed at different angles when binding to antigens

56
Q

do all antigens have a hinge region?

A

no

57
Q

an antigen and its complementary antibody have…

A

complementary molecular shapes, this means that their molecular structures fit into each other

58
Q

what happens when an antibody collides (randomly) with a foreign cell that possesses non-self antigens with a complementary shape?

A

it binds with one of the antigens & forms an antigen-antibody complex

59
Q

how many antigen-binding sites do antibodies usually have?

A

at least two antigen-binding sites

60
Q

how many foreign cells can an antibody bind to at once?

A

more than one

61
Q

agglutination

A

when an antibody binds to more than one foreign cell at a time, causing groups of the same pathogens to become clumped together

62
Q

what does the binding of antibodies to antigens do?

A

-neutralises the pathogen
OR
-acts like a marker to attract phagocytes to engulf and destroy the pathogens

63
Q

what do memory cells for the basis of ?

A

immunological memory

64
Q

define immunological memory

A

the ability of the immune system to quickly and specifically recognize an antigen that the body has previously encountered and initiate a corresponding immune response

65
Q

how long do memory cells usually last?

A

many years and often a lifetime

66
Q

what are the two types of immune responses?

A

-primary immune response
-secondary immune response

67
Q

define primary immune response

A

responding to a newly encountered antigen (relatively slow)

68
Q

define secondary immune response

A

responding to a previously encountered antigen (quicker)

69
Q

steps of a primary immune response

A

1) after clonal selection and expansion, the b-lymphocytes that have become plasma cells secrete lots of antibody molecules

2) these plasma cells are short-lived, but the antibodies they have secreted stay in the blood for a longer time

3) the other b-lymphocytes become memory cells that remain circulating in the blood for a long time

70
Q

steps of a secondary immune response

A

this response relative to the primary immune response is extremely fast!!

1) if the same antigen is found in the body a second time, the memory cells recognise the antigen, divide very quickly and differentiate into plasma cells (to produce antibodies) and more memory cells

2) this response is very quick, meaning that the infection can be destroyed and removed before the pathogen population increases too much and symptoms of the disease develop

71
Q

what two sections are defence mechanisms split into?

A

-specific
-non- specific

72
Q

what is a non specific response & longevity?
(+ examples)

A

-mechanisms that do not distinguish between pathogens, but respond to all of them in the same way.
-these mechanisms act immediately

( physical barriers, phagocytosis)

73
Q

what is a specific response & longevity?

A

-mechanisms that distinguish between different pathogens
-the response is less rapid but provides long lasting immunity

74
Q

define cell mediated response

A

an immune response that does not involve antibodies, primarily driven by t cells

75
Q

define humoral response

A

produces antigen-specific antibodies and is primarily driven by b cells

76
Q

what are vaccines?

A

-antigens that cause your body to produce memory cells against a particular pathogen, without the pathogen causing disease
-this means you become immune without getting any symptoms

77
Q

the two types of vaccines:

A

1) dead
2) attenuated (weakened)

78
Q

how are vaccines administered?

A

by injection (into vein/muscle) or orally

79
Q

disadvantages of taking a vaccine orally

A

it could be broken down by enzymes in the gut or the molecules of the vaccine may be too large to be absorbed into the blood

80
Q

how can vaccinations produce long term immunity?

A

-they cause memory cells to be created
-the immune system remembers the antigen when reencountered and produces antibodies to it faster

81
Q

benefits of vaccines:

A

1) highly effective with one vaccination giving a lifetime’s protection (less effective ones will require booster)

2) generally harmless as they do not cause the disease they protect against

82
Q

disadvantages of vaccines

A

1) people can have a poor response (eg. they are malnourished and cannot produce the antibodies or their immune system may be defective)

2) antigenic variation – the variation in the antigens of pathogens causes the vaccines to not trigger an immune response/diseases caused by eukaryotes have too many antigens on their cell surface membranes making it difficult to produce vaccines that would prompt the immune system quickly enough

3) antigenic concealement - occurs when the pathogen ‘hides’ from the immune system by living inside cells / when the pathogen coats their bodies in host proteins / by parasitising immune cells / remaining in parts of the body that are difficult for vaccines to reach

83
Q

what are attenuated vaccines?

A

vaccines that whole pathogens that have been ‘weakened’

84
Q

how do attenuated vaccines work?

A
85
Q

benefits of attenuated vaccines

A

tend to produce a stronger and longer-lasting immune response

86
Q

disadvantages of attenuated vaccines

A

-can be unsuitable for people with weak immune systems, the pathogen may divide before sufficient antibodies can be produced

87
Q

examples of attenuated vaccines

A

MMR

88
Q

what is a dead/inactivated vaccine?

A

-contain whole pathogens that have been killed or subunit’s of the pathogens
-do not contain living pathogens they cannot cause disease

89
Q

benefits of dead vaccines

A

they cannot cause disease, even for those with weak immune systems

90
Q

disadvantages of dead vaccines

A

-do not trigger a strong or long-lasting immune response
-booster doses are often required
-some people may have allergic reactions or local reactions to inactivated vaccines as adjuvants may be joined to the subunit of the pathogen to strengthen and lengthen the immune response

91
Q

examples of dead vaccines

A

whole → polio vaccine
subunit → diphtheria

92
Q

what is herd immunity?

A

when a sufficiently large proportion of the population has been vaccinated which makes it difficult for a pathogen to spread within that population

93
Q

why is herd immunity important?

A

it allows for the individuals who are unable to be vaccinated (e.g. children and those with weak immune systems) to be protected from the disease

94
Q

how does herd immunity vary?

A

the proportion of the population that needs to be vaccinated in order to achieve herd immunity is different for each disease

95
Q

issues with eradicating disease:

A

-some pathogens are complicated and so a successful vaccine has not been developed
-a diseases that could be eradicated where a vaccine does exist, hasn’t been eliminated because too few in the community have been vaccinated
-unstable political situations
-lack of public health facilities

96
Q

what is active immunity?

A

antigen enters the body triggering a specific immune response (antibodies are produced)

97
Q

how can active immunity be acquired?

A

-through exposure to microbes
-artificially acquired through vaccinations

98
Q

during the primary response to a pathogen how long does the antibody concentration in the blood take to increase?

A

one to two weeks

99
Q

what is passive immunity?

A

acquired without an immune response. antibodies are not produced by the infected person

100
Q

passive immunity & secondary immune responses

A

as the person’s immune system has not been activated then there are no memory cells that can produce antibodies in a secondary response, if a person is reinfected they would need another infusion of antibodies

101
Q

when does artificial passive immunity occur?

A

when people are given an injection / transfusion of the antibodies

102
Q

when does natural passive immunity occur?

A

when:
-foetuses receive antibodies across the placenta from their mothers

-babies receive the initial breast milk from mothers which delivers a certain isotype of antibody

103
Q

how is HIV spread? (+ examples)

A

by direct exchange of body fluids:

-sexual intercourse
-blood donation
-sharing of needles by drug users
-from mother to child across the placenta
-mixing of blood between mother and child during birth
-from mother to child through breast milk

104
Q

components of HIV

A

-two RNA strands
-proteins (including the enzyme reverse transcriptase)
-capsid
-viral envelope consisting of a lipid bilayer and glycoproteins
-attachment proteins

105
Q

when viruses enter the bloodstream what cell do they infect?

A

t helper cells

106
Q

how does HIV avoid being recognised and destroyed by lymphocytes?

A

by repeatedly changing its protein coat

107
Q

HIV replication steps:

A

1) hiv attaches to receptors on
t-lymphocytes

2) hiv injects it’s genetic material into the lymphocyte, which becomes a host

3) reverse transcriptase enzymes produce a DNA copy of the viral RNA, the DNA copy is inserted into the chromosomes of the cell

4) each time the cell divides it copies the viral DNA

5) the infected cells remain normal as the viral DNA is inactive

108
Q

what happens after years when viral DNA within the host cells becomes active?

A

-it takes control of the helper t cell so more HIV particles are produced &
the helper t cell dies
-thousands of new HIV particles are released which canto infect other helper t cells

-gradually the virus reduces the number of t helper cells in the immune system
-b cells are no longer activated, no antibodies are produced
-this decreases the body’s ability to fight off infections

109
Q

symptoms of AIDS

A

-mild flu-like symptoms after HIV infection

110
Q

when are people said to have AIDS?

A

when they can no longer produce antibodies and fight off infections

111
Q

what are opportunistic diseases?

A

diseases that would usually cause very minor issues in healthy individuals that cause an individual with advanced AIDS to die

112
Q

treatment of AIDS

A

antiretrovirals that slowing the spread of the virus within the body / delay the development of AIDS in those with HIV

113
Q

what are antibiotics used for?

A

-to kill bacteria or limit bacterial growth

114
Q

what are antibiotics ineffective against?

A

viruses

115
Q

HIV vs AIDS

A

-HIV is a virus
-AIDS is the disease caused by HIV

116
Q

uses of monoclonal antibodies:

A

-pregnancy tests
-diagnosing HIV
-detecting the presence of pathogens
-detecting the presence of antibiotics in milk
-detecting cancer cells

117
Q

how many times are monoclonal
antibodies used?

A

generally only once

118
Q

how monoclonal antibodies are used to detect HIV: (steps)

A

1) the hiv antigen is attached to a test plate

2) the blood sample being tested is passed over the test plate. if hiv antibodies are present they bind to the antigen. the plate is then washed

3) a monoclonal antibody is then passed over the plate. its antigen is the hiv antibody and it will bind to it if it is present. the monoclonal antibody is attached to an enzyme

4) the bound monoclonal antibody is proportional to the bound hiv antibody. a dye called chromogen is passed over the plate. the enzyme catalyses a colour change in the dye. the more intense the colour on the plate, the more hiv antibody present in the test serum

119
Q

therapeutic uses of monoclonal antibodies

A

-treatment for the rabies virus
-the prevention of transplanted organ rejection
-autoimmune therapies
-prevention of blood clotting
-targeted treatment of breast cancer
-prevention of blood clotting
-treatment of melanoma

120
Q

how is rabies treated with monoclonal antibodies?

A

by injecting purified antibodies

121
Q

how is the prevention of transplanted organ rejection achieved with monoclonal antibodies?

A

by intervening with the T cells involved in the rejection process

122
Q

how are monoclonal antibodies used in autoimmune therapies?

A

monoclonal antibodies bind to and deactivate factors involved in the inflammatory response

123
Q

how are monoclonal antibodies used to treat breast cancer?

A

herceptin recognises receptor proteins on the surface of cancer cells and binds to them allowing the immune system to identify and destroy them

124
Q

ethical issues associated with the use of vaccines

A

-use of animals
-human testing
-side-effects
-epidemics

125
Q

vaccine ethics: use of animals

A

-all vaccines are tested on animals before they can move onto human-trials
-animal-based substances are sometimes used in the production of vaccines

126
Q

vaccine ethics: human testing

A

-even at the human-trial stage, a vaccine carries a small risk

-volunteers may be at higher risk of contracting the disease if they think the trial vaccine will fully protect them but it actually doesn’t (e.g. they might have unprotected sex because they have had a trial HIV vaccine but they actually end up contracting the disease as a result)

-human volunteers are often paid to take part in vaccine trials, ethical issues can arise if these volunteers feel pressured into doing this (i.e. people who are struggling financially)

127
Q

vaccine ethics: side effects

A

-some people refuse to take a particular vaccine due to the possibility of side effects, these people are often protected due to herd immunity, other people may think this is unfair

-some parents refuse to let their children be vaccinated - should a parent be allowed to put their child at risk?

128
Q

vaccine ethics: epidemics

A

-when new pandemics occur there is often a struggle as to who should be vaccinated first
-there is also often a struggle between countries as to who receives the vaccines first and in what quantities

129
Q

ethical issues associated with the use of monoclonal antibodies

A

-new monoclonal antibody therapies are often tested on animals before they can move onto human-trials

130
Q

define monoclonal antibodies

A

identical copies of one type of antibody

131
Q

what does ELISA stand for?

A

enzyme-linked immunosorbent assay

132
Q

what are ELISA tests used to do?

A

to see if a patient has any antibodies to a certain antigen

133
Q

two different types of ELISA tests

A

-direct
-indirect

134
Q

direct ELISA test

A

use a single antibody that is complementary to the antigen being tested for

135
Q

indirect ELISA tets

A

use two different antibodies

136
Q

steps of ELISA test for HIV:

A

1) HIV antigens are bound to the bottom of the reaction vessel

2) a blood plasma sample is then taken from the patient and added to the reaction vessel

3) any HIV-specific antibodies that are present in the blood now bind to the HIV antigens, these HIV-specific antibodies are known as the primary antibodies

4) any other antibodies that are present in the blood plasma are unbound and are washed out

5) second type of antibody with an enzyme attached to it is added to the reaction vessel (secondary antibodies),
these secondary antibodies bind to the primary antibodies

6) the reaction vessel is washed out again to remove any unbound secondary antibodies (this is important in avoiding false-positive test results, If they are not washed out, unbound secondary antibodies would give a positive result, even if there were no primary antibodies present to start with)

7) a solution is added that contains a substrate that reacts with the enzyme attached to the secondary antibodies. if there are any secondary antibodies present, a coloured product is formed, causing the solution in the reaction vessel to change colour. this indicates that the patient has HIV

137
Q

ELISA TESTING: prostate cancer

A

1) antibodies to PSA are both to the bottom of the reaction vessel

2) blood plasma sample is added & then washed out

3) secondary antibody (with an enzyme attached) is added, it only binds to primary antibody if PSA is present

4) substrate is added & the enzyme reacts with substrate forming a coloured product, the colour change means that PSA is present

A LEVEL BIO (12 decks)

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