12.8 Immunology Flashcards
1
Q
state 2 ways that pathogens cause harm / disease
A
- pathogens can produce toxins which can directly damage tissue
- pathogens can sometimes replicate inside and destroy host cells
2
Q
each type of cell has … on its plasma cell-surface membrane that identify it
A
specific molecules
3
Q
these molecules include proteins and enable the immune system to identify:
A
- pathogens
- cells from other organisms of the same species
- abnormal body cells (cancer cells from on body)
- toxins (often secreted by pathogenic bacteria)
4
Q
antigen definition
A
a molecule (usually a protein) that stimulates an immune response that results in the production of a specific antibody (antibody generator)
5
Q
own cells =
A
SELF
6
Q
foreign cells / pathogens =
A
NON SELF
7
Q
the surface of all own cells (self) and foreign cells / pathogens (non self) are covered in…
A
specifically shaped antigens
8
Q
these antigens help identify…
A
each particular type of cell to the host organism
9
Q
what happens if the antigens are not recognised
A
the body will treat that cell / pathogen as non self and initiate an immune response which will lead to the destruction of the cell / pathogen / protein.
10
Q
examples of antigens
A
glycoproteins and glycolipids
11
Q
what are phagocytes
A
groups of white blood cells which can distinguish between cells which do or do not display the self-antigens
12
Q
the process phagocytes undergo is called
A
phagocytosis
13
Q
phagocytosis process
A
- pathogen is engulfed by the phagocyte
- engulfed pathogen enters the cytoplasm of the phagocyte in a vesicle which is now called a phagosome
- lysosomes fuse with phagosome releasing hydrolytic digestive enzymes (lysozymes)
- lysosome enzymes hydrolyse the pathogen
- waste materials are released from the cell by exocytosis and antigens presented on the cell surface membrane and the phagocyte becomes an antigen presenting cell (APC)
14
Q
is phagocytosis specific or non-specific
A
non-specific (works the same for any pathogen that displays a non-self antigen)
15
Q
why is phagocytosis not used in the event of an infection
A
- it would take far too long to destroy all the invading pathogens
- may result in damage to tissues and organs
16
Q
name the specific cellular responses
A
- response of T lymphocytes (cell-mediated immunity -> primary response)
- action of T cells
- activation of B cells (humoral response -> primary response)
17
Q
2 stages in response of T lymphocytes (cell-mediated immunity -> primary response)
A
- antigen presenting
- clonal selection
18
Q
antigen presenting process in response of T lymphocytes (cell-mediated immunity -> primary response)
A
- specific TH cells can respond directly to a specific pathogen or its antigens / respond to APC that presents the specifically complementary antigen to their receptors
- APC presents the pathogen’s antigen on its cell surface membrane
19
Q
clonal selection process in response of T lymphocytes (cell-mediated immunity -> primary response)
A
- a specific TH cell binds to presented antigen via its complementary receptor
- TH cell is activated and clones to produce many TH cells with complementary receptors to the antigen
20
Q
summary of the process: response of T lymphocytes (cell-mediated immunity -> primary response)
A
- phagocyte engulfs & hydrolyses the pathogen and presents the antigen on its cell surface membrane
- TH cell with specific receptor molecule binds to presented antigen
- once TH cell binds to the presented antigen it is activated. it then rapidly clones by mitosis
21
Q
roles of the TH cell
A
- specific TH cell binds to the APC
- release cytokines that attract phagocytes to the area of infection
- release cytokines that activate TC cell (cytotoxic killer)
- activates a specifically complementary B cell
- form memory TH cell
22
Q
roles of the TC cell (cytotoxic killer)
A
- locate and destroys infected body cells that present the corrected antigen
- binds to APC
- releases perforin (protein) which creates holes in the cell surface membrane which destroys the APC
23
Q
what is the humoral response
A
involves the activation of B cells to produce antibodies. B cells must be stimulated by their complementary TH cell by the release of cytokines.
24
Q
stages in the process: activation of B cells (humoral response -> primary response)
A
- B cell activation
- (B cell differentiation)
25
B cell activation process in activation of B cells (humoral response -> primary response)
- a specific TH cell with the correct receptor binds to presented antigen and then locates and activates a specifically complementary B cell
- the specific TH releases cytokine chemicals that signal the specific B cell to clone by mitosis (clonal selection)
26
what 2 types of cell do B cells differentiate into
- plasma cells
- memory B cells
27
role of the plasma cells
produce and secrete vast quantities of specific antibodies into the blood plasma
28
role of the memory B cells
remain in the body to respond to pathogen rapidly ad extensively should there be a future re-infection
29
antibody definition
protein made in response to foreign antigen - has binding sites which bind specifically to an antigen. a specific antibody is produced by a specific plasma cell
30
structure of the antibodies
- complex proteins
- quaternary structure
- 4 polypeptide chains
31
shape of the antibodies
'Y shaped'
32
what is the main part of the antibodies called that is the same in all antibodies
constant region
33
what is different in all the antibodies
variable region
34
structure of the variable regions
- different primary structure
- different tertiary structure
- different shapes
35
what characteristic of the variable region causes the antibodies to be specific
- specific binding site (different for each antibody)
- therefore specific antibodies are only complementary to 1 antigen
36
when specific antibodies bind to specific antigens due to having specific binding sites, what do they form
(permenent) antigen-antibody complex
37
role of the antibodies in destruction of pathogens
- agglutination
- opsonisation
- lysis
- anti-toxin + anti-venom
- prevent pathogen replication
38
agglutination meaning
specific antibodies bind to the antigens on pathogen clump them together
39
opsonisation meaning
marking pathogens so phagocytes recognise and destroy the pathogen more efficiently
40
lysis meaning (anitgens)
bind to antigens and lead to destruction of the pathogen's membrane
41
anti-toxin + anti-venom meaning
bind to toxins or venom (both usually proteins) to prevent these molecules from binding to their complementary target receptors
42
are memory B cells involved directly in destroying the invading pathogen
no
43
process that memory B cells undergo when they encounter the antigen again
- if the memory cells encounter the antigen again, they are rapidly activated (by cytokines secreted by specific TH cell) and divide rapidly by mitosis
- the genetically identical cloned memory cells differentiate into plasma cells and (even) more memory B cells
- the plasma cells produce vast numbers of the specific antibodies for the invading pathogen, in a short period of time
44
secondary response meaning
the activation of memory cells to produce antibodies
45
the secondary response is both...
rapid and extensive
46
in the secondary response, the antigen is normally...
eliminated before it can cause disease or any symptoms to develop
47
key point to remember in a secondary response
more antibodies are produced more rapidly
48
is the immune response more effective or less effective
more effective
49
why is the immune response more effective
most pathogens have the same antigens on their surface, and so are recognised by memory cells when re-infection occurs
50
why might an individual not be able to initiate a secondary response
gene mutations in pathogens may lead to change in tertiary structure of antigens specific to the B cell, meaning memory B cell antibodies will no longer be complementary to the mutated pathogen so non antigen-antibody complex will form and the individual will not be able to initiate a secondary response
51
what is a change in an antigen called
antigenic variability (drift)
52
what does antigenic variability mean when developing vaccines
makes it difficult to develop vaccines against these pathogens
53
what are the 2 ways in which immunity can be gained
passive immunity and active immunity
54
characteristics of passive immunity
- no exposure to antigen
- antibodies are given (mother, antiserum)
- no memory cells are produced
- short term
- fast acting
55
characteristics of active immunity
- exposure to antigen
- antibodies are produced
- memory cells produced
- long term
- takes time to develop
56
what do vaccines contain
antigens from dead, weakened or attenuated pathogens
57
process of a vaccination
- the pathogen is engulfed by a phagocyte and displayed on an APC
- a specific TH cell binds to the antigen on the APC
- the specific TH cell stimulates a specific B cell (by releasing cytokines)
- B cell divides by mitosis to produce plasma cells and memory cells
- plasma cells produce and release antibodies
- memory cells recognise the antigen on second infection
58
vaccines are not effective against what
pathogens which show antigenic variability
59
what 4 things can vaccinations be and examples
- antigens isolated as fragments of the pathogen (HPV)
- weakened / attenuated heat treated versions of the pathogen (MMR / live bacterium but not pathogenic)
- inactivated toxin from pathogen (tetanus vaccine)
- killed pathogen (whooping cough vaccine)
60
some vaccinations are known to cause...
side effects
61
these side effects are usually...
mild and cause fewer problems / complications than the disease itself
62
however in some individuals these side effects may result in...
complications which have severe (permanent) effects on the individual
63
taking the vaccine or not is the decision of who
the decision of individuals (with medical advice)
64
herd immunity definition
if enough individuals in the population are vaccinated (85%), then there is little chance of the disease spreading, therefore even non-vaccinated individuals will be protected
65
ethical issues associated with vaccines and their development
- development and testing involve use of animals...does this infringe rights of animals?
- human testing...who should be tested, are they being put at possible risk? is this justified by possible benefit to society?
- is it available to all or only those who can afford it? (in this country, in 3rd world etc)
- balancing risk of side effects against possible benefit
- should vaccination programmes be compulsory, if society benefits?
- should we be aiming to eliminate an organisation? (loss of genetic variability)
66
monoclonal antibodies definition
- antibodies with the same tertiary structure
- artificial antibodies that are produced from a single clone of cells by fusing B-lymphocytes to myeloma cells.
67
uses of monoclonal antibodies
- research
- immuno assays (pregnancy testing kits and ELISA)
- diagnosis (showing presence of a particular antigen)
- targeting drugs
- killing specific cells (abnormal cancer cells)
- isolating specific chemicals
68
purpose of ELISA tests
used to determine the presence of the antibody (indirect ELISA) or the antigen (sandwich ELISA)
69
process of indirect ELISA
- antigen-coated well
- wash
- specific antibody binds to antigen
- wash
- enzyme-linked antibody binds to specific antibody
- wash
- substrate is added and converted by enzyme into coloured product; the rate of the colour formation is proportional to the amount of specific antibody
70
process of sandwich ELISA
- antigen-coated well
- wash
- add antigen to be measured
- wash
- add enzyme-conjugated secondary antibody
- wash
- add substrate and measure colour
71
what does HIV stand for
human immunodeficiency virus
72
HIV causes what disease
AIDS
73
what is HIV made up of
- attachment proteins
- lipid envelope
- capsid
- reverse transcriptase
- HIV RNA (2 identical strands)
74
process of HIV replication - using TH cells
- attachment proteins on HIV binds with a protein receptor commonly found on TH cells
- capsid fuses with cell surface membrane and releases viral RNA and enzymes into the helper TH cell
- the HIVs reverse transcriptase converts viral RNA into cDNA using host nucleotides and cDNA converted to dsDNA by DNA polymerase
- viral cDNA moves into nucleus of T cell and is inserted into host cell genome (DNA). the person / cell is now infected.
- transcription of viral DNA into (viral) mRNA which is translated to produce HIV proteins. the infected TH cell starts to manufacture new HIV virions / particles
- particles (virions) break away from TH cell with a section of host cell surface membrane which forms their lipid envelope, with TH receptor proteins embedded (to gain access into more TH cells).
75
over time what does the process of HIV replication - using TH cells
leads to a reduction in the number of TH cells or reduction by inactivation of TH cells
76
what does AIDS stand for
acquired immune deficiency syndrome
77
is aids a pathogen
no
78
as aids is not a pathogen what does this mean
it cannot be detected using antigens or antibodies
79
how is aids detected
can be screened for by checking the number of TH cells
80
what is compromised due to HIV using TH cells
cell mediated immunity is compromised as HIV reduces an individuals ability to respond to pathogens
81
how many TH cells should an uninfected person have in their blood
800 - 1200 TH cells mm-3 of blood
82
how many TH cells should a person suffering from AIDS have in their blood
few as 200 TH cells mm-3 of blood
83
what does screening ELISA for HIV antibodies do
can be used to determine the HIV status of a patient
84
does HIV kill directly
no
85
how does HIV kill indirectly
compromises the immune system so it leaves people vulnerable to secondary diseases that ultimately causes death
86
how are people left vulnerable to secondary diseases
B memory cells must be activated by specific TH cells, which may have been destroyed
87
what does many AIDS sufferers develop
infections of lungs, intestines, brain, eyes, weight loss, diarrhoea (symptoms)
88
AO2 Qs - AIDS
- more HIV
- destruction of more TH cells
- less activation of (specific) TC / B cell
- less able to destroy (other) pathogen / cancerous / infected cell
89
how do antibiotics work
- prevent bacteria making a normal cell wall (murein / peptidoglycan) by targeting 70s ribosomes
- means bacteria are unable to resist osmotic pressure and the cells burst due to an increase in cell volume of water by osmosis
90
why do antibiotics not act on viruses
viruses:
- use host cells organelles to carry out metabolic activities so don't have any viral organelles to disrupt
- have a capsid (protein coat) rather than murein cell wall
- spend most of the time within a host cell so out of reach of antibiotics
