1
Q
What are fungi?
A
- cellular pathogen
- eukaryotic organisms (yeast, moulds, mushrooms)
- unicellular or multicellular
- often found in high moisture environments
- mostly affect external surfaces of individuals
2
Q
What is a pathogen? What are the types of pathogens?
A
infectious agent that causes disease
cellular: living organism (composed of cells) that causes disease to a host, can reproduce independently
non-cellular: disease-causing agent that lacks cellular structures and cannot replicate outside host cell, non-living
3
Q
What are bacteria?
A
- cellular pathogen
- prokaryotic and unicellular
- cause disease by:
producing toxins that build up and affect cellular functioning
damage host cells directly
interfere with immune system cells - can divide rapidly inside host
growth graph shape– exponential as replicate by binary fission
4
Q
What are superbugs?
A
- subset of bacteria
- superbug is an organism that has developed resistance to antibiotics
5
Q
What are protozoa?
A
- cellular pathogen
- eukaryotic and unicellular
- moist environments (waterways, soil)
- have features like cilia or flagella making them highly mobile
- free living or parasitic
- do not have many drugs or vaccines for treatment
6
Q
What are prions:
A
- pathogenic protein with a mutant structure that can trigger normal proteins to fold abnormally into more prions
- unique as pathogens as they do not contain any genetic material and cause disease by toxic build up of tissue
- resistant to high temps (don’t denature), strong enzymes and radiation
- untreatable and fatal (cannot destroy prions w/o causing harm to patient– ((AND immune system does not defend against prions because they are not recoginsied as foreign- no immediate innate immune response to stimulate adaptive immune system))
7
Q
What are viruses?
A
- force host cells to produce thousands of identical copies of virus, which infect new host cells, disrupting cellular function
- obligate- cannot survive long outside host cell, need host cell to replicate
All contain two features: - Genetic material (DNA or RNA)
- protective protein shell called a capsid
(growth graph shape– viruses are intracellular and extracellular- numbers plateau while they are inside the cell replicating, and increase in numbers when infected cells lyse)
8
Q
Reproduction mechanism of virus:
A
- Attachment and entry
- Bind to cell surface receptors and enter - Uncoating
- virus removes its protein coat and nucleic acid is released - Replication and gene expression
- virus uses host cell machinary to replicate its nucleic acid and transcribe and translate viral proteins. - Assembly
- new viral genomes and proteins are assembles into viral particles - Release
- viruses are released into extracellular fluid (often cell is lysed and dies)
- new virus particles bind to surrounding cells and repeat the process
9
Q
Disease: modes of transmission (infectious)
A
Direct:
- immediate transfer of infectious agents to host
- direct contact (handshaking, body fluid exchange)
- droplet spread (at close range), sneezing
- touching contaminated surface
Indirect:
- spreads via something else first
(via water, food, vectors, host animals)
10
Q
What is disease? and types
A
- any condition that affects the normal functioning of an organism (dysfunctionality)
Non-infectious:
- not caused by a pathogen
- cannot be directly transmitted between organisms
- not contagious / non-communicable
- caused by genetics, lifestyle
infectious:
- caused by a pathogen
- transmitted between organisms directly or indirectly
- most are contagious: transmitted from one HUMAN to another, some are not
- communicable: transmitted from one organism to another
11
Q
Vector vs carrier
A
Vector (indirect)
- living organims that carry and transmit pathogens
- not affected itself by pathogen
e.g. mosquitos not affected by parasite
Carrier: (indirect)
- organism that is infected by the pathogen and can trasnmit it to another organism
- usually symptomatic
12
Q
Course of disease:
A
- Incubation (between exposure to pathogen and first appearance of symptoms)
takes time as:
- pathogens need to replicate enough to cause disease
- needs to reach target tissues (further away in body- more time)
- toxins released by pathogen needs to accumulate - symptoms of disease
- recovery
3 lines of defence (natural immune system response) or prescribed medicine
13
Q
What are antigens?
A
- unique molecule on the surface of a cell to distinguish that cell from cells of other organisms
(technically antigen is a molecule that elicits an immune response (foreign) but vcaa says self-markers=self antigen)
14
Q
types of Self-markers / antigens
A
MHC class 1 markers:
found in every nucleated cell (all cells except red blood cells)
help distinguish between self and non self antigens
MHC class 2 markers:
- only found on antigen presenting cells
- part of adaptive response to defend against pathogens
15
Q
Non-self antigens
A
- molecules on surface of pathogens that initiate an immune response
- different depending on pathogen
- pathogen can have different antigens
16
Q
What is an allergen:
A
- any stimulus that triggers an allergic reaction (different people- different allergens)
- allergic reaction: result of overreaction by body’s immune system to a normally harmless substance.
17
Q
Outline the first line of defence
A
- innate (non-specific, rapid, don’t need prior exposure to pathogen)
Physical barriers: prevent entry of pathogen into organism
chemical barriers: reduce pathogen’s ability to grow
microbiota: compete pathogen for resources and space, preventing growth and reproduction
18
Q
Examples of first line of defence: physical
A
in animals:
- intact skin
- hair
- epithelial cells
- cilia and mucous lining in respiratory system (trap and sweep out pathogens)
plants:
- thickened cell wall (or not?)
- intact and waxy cuticles
- stomata can be closed when signalled
- thorns
- thick bark
- vertical orientation of leaves (prevents water and pathogens collecting)
- formation of galls (limits spread of pathogen)
19
Q
Examples of first line of defence: chemical barriers
A
Animals:
- sweat (secreted by skin, contains salt which inhibits bacteria)
- tears and saliva (contain lysozyme enzymes which cause bacteria to lyse)
- surfactants (in lungs- coat pathogen making it easier for elimination by phagocytes)
- stomach acid (breaks down bacteria)
Plants:
- secretion of enzymes that digest pathogens
- secretion of antibiotic-like (OR antimicrobial?) substances (fungicides and toxins) that kill pathogens before they can enter plant cells
- resin
- saponin (in wheat- disrupts cell membrane in fungi)
- caffeine (coffee plants- toxic to insects and fungi)
20
Q
Microbiota
A
- animals only
- known as microflora
- non-pathogenic bacteria found on skin, mouth, nose, digestive tract, vagina
- prevent growth and colonisation of bacteria by:
- competing with other bacteria for space and resources
- producing chemicals that reduce the pH of the micro-environment
- antibiotics do not discriminate between beneficial flora and harmful bacteria—- disrupt normal flora and gut function
21
Q
characteristics of the second line of defence
A
- non-specific
- rapid (within mins-hours)
- fixed
- No immunological memory (of pathogen)
- actions of immune cells and soluble proteins
22
Q
Molecules: second line of defence
A
Cytokines:
- broad group of signalling proteins
- nearly all nucleated cells can produce them
Chemokines:
- type of cytokine
- released by infected cells to attract leukocytes
- leukocytes move against concentration gradient of chemokines
Interferon:
- type of cytokine
- released by virus infected host cells
- protects surrounding cells through helping inhibit viral protein synthesis (surrounding cells receive signals, increasing production of antiviral proteins to prevent viruses from entering cells)
- signal surrounding infected cells to undergo apoptosis
- attracts natural killer cells to kill virus infected cells
23
Q
cells- phagocytosis: second line of defence AND APCs
A
All do phagocytosis:
- microbe binds to membrane
- phagocyte engulfs microbe, forming a phagosome (vesicle with pathogen)
- phagosome fuses with lysosome, forming a phagolysosome
- lysosomes have enzymes that digest bacteria
- some atoms are used by cell
- indigestible material expelled into extracellular fluid
- some fragments bind to MHC-11 marker in cytoplasm, forming antigen-MHC-II complexes which are displayed on cell surface
24
Q
cells- neutrophils: second line of defence
A
Neutrophils
- circulate in the blood (first responders in response to signals from other cells)
- leave blood vessels, attracted to site of infection by chemokines
- fast-acting
function:
- engulf pathogen by phagocytosis
- contain granules that release cytotoxic chemicals (defensins), to target and disrupt bacterial and fungal membranes.
- Release cytokines to attract more immune cells.
- involved in inflammation
- after phagocytosis, undergo apoptosis
25
cells- macrophages: second line of defence
- found in body tissues
- attracted to infection site by cytokines
function:
- engulf pathogen via phagocytosis and breaking it down
- keeps the antigen (puts it on surface membrane- memory if bacteria invades again)
- acts an antigen presenting cell (APC) - link to activation of the cell-mediated response in the third line of defence.
- Release cytokines.
26
cells- dendritic cells: second line of defence
- many grooves - increase surface area and permit contact with a large number of nearby cells.
- Found in body tissues
function:
- Engulf pathogens by phagocytosis.
- Break down pathogens and retain antigens (antigen presenting cells)
- release cytokines
27
Natural Killer cells: 2nd line of defence
- cytotoxic cell
- destroy virally infected or damaged AND cancerous cells
- recognise targets through absent or damaged MHC-Class 1 markers (cancer and viruses reduce transcription of MHC- class 1)
- release cytotoxic chemicals, such as perforin, that cause holes in the plasma membrane and granzymes, that trigger cell death (apoptosis)
- release cytokines to attract specific adaptive immune cells
- if enough mutations accumulate, NK cells may not be able to kill target cell (due to loss of activating signals, cell upregulating transcritpion of MHC markers)
28
2nd line of defence: Eosinophils
- have granules which contain cytotoxic chemicals that target parasites
- secrete toxic chemicals
- involved in inflammation / allergic responses
29
2nd line of defence: complement proteins (chemical response)
- set of proteins found in blood
- when activated: bind to CELLULAR pathogens
- damage plasma membrane of bacteria:
form membrane attack complexes on the membrane, creating a pore. This allows water, ions and fluid from blood to flow in, causing swelling and lysis.
this stimulates phagocytic action
- they attract phagocytes to site of infection
- opsonise: coat pathogen and act as flags, making the them more identifiable. (makes phagocytosis faster and more efficient)
- Contribute to inflammation by increasing local permeability of capillaries (assist in vasodilation, allowing immune components to leak out of blood vessels)
- contribute to chemotaxis- attracting immune cells to site of infection
30
The inflammation response: example of splinter
Functions:
- removes harmful stimuli and intitiates the healing process
- confines infection to a small area
- splinter damages tissues
- damaged cells release stress signal which activate mast cells
- mast cells release histamine
- Histamine initiates vasodilation (blood vessels become wider)
- increases blood flow to the site of injury, delivering more immune cells.
- vasodilation also causes blood vessels to become leaky, allows more immune cells to travel out of the blood vessels to site of infection (e.g. neutrophils)
- response continues until cleared of pathogens and debris.
31
symptoms of inflammation:
vasodilation--- increased blood flow (red blood cells released into tissue)----- redness and heat
increased capillary permeability---- fluid enters inflammation site ----fluid buildup leads to swelling
extra fluid applies pressure to nerve endings, causing pain
- pus is fluid containing large amount of dead immune cells (neutrophils), dead tissue debris, and pathogens
32
Role of platelets in wound healing
- platelets are cell fragments in the blood (they are not full cells, break off from larger ones)
- stop the bleeding: if blood vessel is damged, platelets travel to injured area, they clump together to form a plug and stop the bleeding
- help start clotting process
- release cytokines to attract immune cells, and help start inflammation process
33
which molecules and cells are involved in inflammation and which are not?
YES:
- macrophages (release cytokines, phagocytose pathogens and dead cells)
- neutrophils (first immune cells to arrive)
- mast cells
- APCs (phagocytes)
- cytokines
- complement proteins
- dendritic cells (only in chronic inflammation?)
not really:
not for main inflammation: - eosinophils (for allergic reactions and parasite infections)
NO:
- NK (not really involved as mainly antiviral role)
- interferons
34
What is the lymphatic system?
- large network of vessels through which lymph flows through
lymph: pale fluid containing high concentrations of leukocytes
- forms important component of immune and circulatory systems
35
Structure of lymphatic system:
- lymphatic capillaries (smaller, collect tissue fluid/lymph)
- lymph
- lymphatic vessels
- primary lymphoid organs (production and maturation of lymphocyes, includes bone marrow and thymus)
- secondary lymphoid organs (maintenance of mature lymphocytes, activation of adaptive immune response, e.g lymph nodes, spleen, tonsils)
36
what are leukocytes? What are lymphocytes?
- also known as white blood cells
- protect body against pathogens and foreign material
(phagocytes, mast cells, NK, eosinophils, B and T lymphocytes)
- lymphocytes are a type of leukocyte: B and T cells
37
lymphatic flow:
- lymphatic capillaries have thin walls
- rely on muscle movements to squeeze lymph through
- lymph vessels have one-way valves--- lymph fluid moves in one direction- away from tissues and towards lymph nodes
38
Main functions of lymphatic system:
- transport system (for APC to lymph nodes for antigen recognition)
- removal of fluid containing pathogen and antigen fragments from tissues to lymph nodes
- location of lymphocyte development and maturation
- location for clonal selection that initiates the adaptive immune response
39
Characteristics of adaptive immunity
- specificity: recognise and resond to specific antigens
- immunological memory: cells 'remember' antigen after initial exposure, larger and more rapid response when exposed to same antigen again
(plants do NOT have 3rd line of defence)
40
clonal selection theory
- a specific antigen activates a specific lymphocyte with a complementary receptor
41
clonal expansion
- activated naive lymphocyte proliferates, producing many clones (same genetic material and same receptor - same antigen specificity)
- clones then differentiate into effector cells and memory cells
42
naive B cells
- recognise and bind to one specific antigen (clonal selection)
- receptors on naive B cells are complementary to their antigens
43
B Plasma cells
- effector B lymphocytes
- result from: naive B cell is activated and goes through clonal expansion (most expanded B cells are effector)
- secrete specific antibodies against the same antigen that activated the original naive B cell
44
Memory B cells
- same antibody surface receptors/(antigen receptor) as original naive B cell
- remain in lymph tissue for long periods, aiding in long term immunity / provides immunological memory (so that a more rapid and larger response producing more antibodies during secondary infection)
- (clone of original naive b cell- but not exact copies- as it has same antibody receptor- allows second response to be faster as there is no initial selection- only clonal expansion)
45
antibodies: what are they
- immunoglobulin (type of protein) (Ig)
- circulate in the bloodstream
- proteins that target and bind to antigens in the extracellular space
- same antigen binding site as the cell surface receptors of the parent naive B cell
46
antibody structure and bonds
- y shaped with 4 polypeptide chains (quaternary)
- 2 heavy + 2 light polypeptide chains
- bonded via disulphide bridges
- stem: constant region
- tips: variable region (both variable regions on same antibody are identical)
antigen binding site (what gives antibody its specificity)- antigen binds to the ends of the variable region
47
Functions of antibodies: neutralisation
neutralisation of pathogens:
- antibodies bind to antigen and form a coating
- prevents pathogens (e.g. viruses) from entering host cells
- bind to toxins and block their actions (usually bacterial toxins)
48
Functions of antibodies: agglutination
- antibodies bind to antigens- antibodies and pathogens clump together by cross linking (one antigen binding site on each pathogen)
- enhances ability of phagocytes to engulf more than one pathogen at once
49
Functions of antibodies: opsonisation
- antibodies bind to antigens and tag them
- constant regions stick out- helps it be recognised by phagocytes - increases phagocytosis
50
Functions of antibodies: activation of complement proteins
- antigen-antibody complex binds to complement proteins, activating them (via constant regions)
- complement proteins form pores on the pathogen membrane, causing them to swell and lyse
- complement proteins promote inflammation and stimulate phagocytosis
51
Outline activation of naive B cells by direct binding of APCs
- APCs go from site of infection to lymph nodes
- using their MHC-II, APCs clonally select a specific B cell whose B cell receptor is complementary to the antigen
- APCs secrete cytokines to help activate the naive B cell
- selected B cell proliferates and differentiates to form many plasma B cells and some memory B cells
- Plasma B cells synthesise and secrete specific antibodies complementary to antigen
- antibodies travel through blood and assist with removal of pathogen by binding to its antigens and attracting phagocytes
- Memory B cells remain in lymph nodes for a long time, only activated if exposed to same pathogen again, providing immunity
52
How do antigen presenting cells work?
- engulf pathogen, take portion of antigen and display it on its membrane
53
Activation of naive B cells through helper T cells
- APCs move from site of infection to lymph nodes
- using their MHC-II, APCs clonally select specific naive T helper cell, whose T cell receptor is complementary to the antigen
- APC release cytokines to help activate helper T cell
- Helper T cell helps to activate a specific naive B cell through cytokine signalling
Plasma B cells synthesise and secrete specific antibodies complementary to antigen
- antibodies travel through blood and assist with removal of pathogen by binding to its antigens and attracting phagocytes
- Memory B cells remain in lymph nodes for a long time, only activated if exposed to same pathogen again, providing immunity
54
What is immunity?
- body's ability to recognise specific pathogens and prevent them from causing illness
55
Active vs passive immunity:
Active:
- produce your own antibodies and memory B and T lymphocytes
- immunological memory is formed
- confers long term immunity
- slow response
Passive:
- passive transfer or antibodies produced by another organism
- no memory cells produced
- adaptive immune system is not activated
- no immunological memory formed
- confers short term protection
- fast, immediate response
56
Types of acquisition of immunity:
1. Natural
- from unintentional or chance encounter with an antigen or antibodies
- pathogen/antibodies enter body naturally
e.g. infection with pathogen (active), maternal antibodies (passive)
2. Artificial
- from intentional introduction of antigens or antibodies into body
e.g. vaccinations (active), monoclonal antibodies, antisnake venom serium-- passive artifical more for when patient is at risk of quick death (passive)
57
Cell mediated immunity: clonal selection and expansion flow chart
Naive T cells (undifferentiated, in lymph nodes waiting to be selected)
Effector cells:
- Helper T cells (Th)
- cytotoxic T cells (Tc)
Memory cells:
- all types of T cells (Th and Tc)
58
Helper T cells
Clonal selection: recognise and bind to specific complementary antigens on MHC-II markers of APC
- APC releases cytokines to activate helper T cell, which undergoes clonal expansion to produce effector Th cells and memory Th cells
59
Effector Th cells
- release cytokines
- help activate cytotocix T cell and naive B cells
60
effector cytotoxic T cells
- directly attack virally infected or cancerous cells by binding to infected cell via MHC-I marker (which act as non self antigens) and releasing cytotoxic chemicals:
- perforin: creates pores in cell membrane, causes lysis
- granzymes: trigger cell to self-destruct
61
activation of cell mediated immunity
1. fragments of virally infected or cancerous cells are taken up by phagocytic APCs
2. APCs migrate to lymph nodes
3. Using their MHC-II, APCs clonally select a specific naive helper T cell whose T cell receptor is complementary to the antigen. The APC released cytokines to help activate the helper T cell
4. selected cell proliferates and differentiates to form effector and memory helper T cells
5. Helper T cells release cytokines, activating them
6. cytotoxic T cells migrate to site of infection, recognise their specific target via MHC-I markers acting as non self antigens, release cytotoxic chemicals that breakdown target cell
7. breakdown of cell attracts phagocytes
62
allergic reactions 1st and 2nd exposure:
1st:
- allergen is phagocytosed by an APC
- APC activates a specific B cell, by direct binding or via a helper T cell
- clonal expansion to create plasma B and memory B cells
- plasma B cells produce IgE antibodies (specific type)
- IgE antibodies bind to mast cells (via heavy chain), sensitising them to a specific allergen
(no symptoms)
future exposure:
- allergen binds to IgE antibodies already bound to mast cells
- histamine is released from mast cells
- inflammatory response initiated
63
What is a vaccine?
- a suspension of dead, attenuated or inactivated pathogens, than when injected, activates the immune system to produce antibodies against the pathogen.
64
viruses vs virions vs viroids
Virus: non cellular agent with genetic material that can replicate only inside a host cell
virion: complete, infective form of a virus outside a host cell (extracellular form of virus)
viroid: short strand of circular, single stranded RNA that has no protein coat, affects mostly plants
65
Disease treatments: antibiotics
- must target only bacteria cells, not human cells
- prevents cell wall forming
- inhibit protein synthesis
- inhibit nucleic acid synthesis or folate acid
- broad spectrum: target wide range of bacteria types
- can also target specific bacteria (narrow range)
- antibiotics may grow resistant
66
Disease treatments: antiviral medication
- target functions and structure that are unique to the virus
- block any part of the reproductive cycle: entering, nucleic acid replication, viral protein synthesis, assemby or release of virions
- one antiviral works on one virus (unlike antibiotics- cell wall similar between bacteria but virus proteins are specific)
- viruses mutate quickly- antibiral may not be effective in a few years
67
Disease treatments: fungicides
- target functions unique to fungi including reproduction
(disrupt nuclear division, nucleic acid synthesis, functions of proteins and enzymes, plasma membrane or cell wall functions)
- specific for each fungus
68
Mechanism of action: vaccines
Primary exposure to vaccine:
- deliberately break 1st line of defence (usually skin)
- vaccine contains specific antigen
- immune system recognises pathogen as having non-self antigens
- body initiate innate immune response (inflammation, APCs)
- stimulates a humoral response, creating memory B cells
- second exposure to non-self antigens (from infection), resulting in a faster and greater number of antibodies produced
- neutralises pathogen before causing disease, producing more memory B cells
69
Booster vaccines:
- initial vaccination produces memory cells and antibodies
- memory cells and antibodies decrease over time
- boosters causes re-exposure to the same antigen:
activates memory B cells which quickly undergo clonal expansion to produce many plasma B cells, which then produce large amounts of antibodies
- produce more memory B cells and antibodies
- allow for faster and stronger immune response to subsequent infection
70
Herd immunity
- large percentage is immune to a disease through vaccination except babies and the vulnerable who cannot be vaccinated
- exact percentage depends on how infectious
- slows spread of disease - lowers chance that an unimmunised person comes into contant with an infectious individual
- protects those who are not immune
- if disease is not severe- can acheive herd immunity through getting disease and recovering
71
endemic:
- disease is constantly present in population
- number of individuals affected is generally low and constant
- limited to a particular region or population
e.g. malaria, chickenpox
72
epidemic
- unexpected rise in disease affecting a large number of people in a specific location or population
e.g. yelloe fever, smallpox, measles, polio
73
pandemic:
- epidemic that has spread over many countries or continents
- generally affects a large number of people
e.g. spanish flu, swine flu
74
Emerging vs re-emerging disease:
Emerging:
- a novel disease caused by a newly identified or previously unknown pathogenic agent
e.g. HIV infections, covid
re-emerging:
- disease was once present
- dramatic decline in case numbers (from genetic chance, vaccines etc)
- disease returns and affects significant proportion of population
e.g. influenza, malaria
75
Ways pathogens can re-emerge:
1. drop of vaccination numbers
- less likely to have herd immunity
2. resistance or evolution of pathogen
e.g. virus changes spike proteins
76
strategies to prevent re-emergence: vaccination programs
- aims to vaccinate enough to stop the spread of disease to eradicate the disease
77
antigenic drift:
- small changes or mutations in virus genes that accumulate over time
- leads to changes in surface antigens
- leads to closely related new strains
- responsible for annual influenza epidemics
- antibodies produced against previous strains may still be effective
78
how diseases re-emerge: bacterial resistance and how to minimise antibiotic resistance
- overuse of antibiotics acts as a selective pressure on bacterial populations
- selects for naturally resistant bacteria
- not antigenic drift
minimise:
- use antibiotics only when necessary and appropriate (not for viruses)
- reduce over prescription of antibiotics by medicine professionals
- reduce overprescription of antibiotics in livestock and fish farming
- complete full course of antibiotics
79
emerging diseases: antigenic shift
- abrupt, major change in a virus
- new surface proteins and new strain
- human and animal viruses co-infect a cell, changing the genetics of the virus, enabling it to infect humans
- forms a new virus subtype
- most people do not have immunity
- may cause pandemics
80
factor affecting emergence of disease
- population growth (closer proximity to others-- more chance of being transmitted)
- close proximity to animals- animals pass on new pathogens to humans
- travel (travelling to uncharted places, encountering new pathogen, easy to spread)
- poverty (low water and sanitation conditions- higher transmission rates)
- climate change (spread to areas may not have previously survived in, release of new pathogens (ice melting))
- antigenic shift
- increased biotecnology (risk of new pathogen escaping)
81
How to prevent the spread of infections:
- good hygiene- washing hands, antibacterial handwash, regularly
- social distancing, infected people are quarantined
- lockdowns or travel restrictions
- fask mask
- getting tested if feeling unwell
- sneezing and coughing in a way that reduces spread of droplets
- cleaning surfaces
public health measures:
- safe and clean water supply
- sewage treatment and disposal
- food safety regulations
- border control of exotic species
- pest and animal control
- quarantine
- vaccination programs
82
What is immunotherapy
- treatment for disease using mAbs
- causes suppression, activation or no effect on immune system
- vaccines also a type
83
What are mAbs?
- antibodies made in the laboratory
84
What is cancer?
- normal cells can turn abnormal in structure (via mutations in genes controlling cell growth)
- mutant cells grow and divide, forming a tumor
- when cells can move, they become malignant
85
What are autoimmune diseases?
- malfunction of the immune system
- immune system is overactive and attacks its own body's tissues
- immune system identifies self cells as non self
- destruction of tissue leads to symptoms of disease
86
side effects of mAbs
- allergic reaction
- rash
- fever
- headaches
- vomiting
- low blood pressure
87
making monoclonal antibodies
1. mouse is injected with an antigen
2. mice's adaptive immune system is stimulated to make B cells that secrete specific antibodies to the target antigen
3. B cells are extracted from mouse's spleen and mouse dies
4. a tumor cell (myeloma) is prepared (because tumor cells divide and grow rapidly and plasma cells are not long lived)
5. B cells are combined with myeloma cells to form a hybridoma
6. Hybridomas have a long life span, can divide quickly and produce large quantities of specific antibodies
7. Hybridomas clone, producing many copies that can produce specific antibody
8. monoclonal antibodies collected and purified
88
mechanisms of action of mAbs:
1. Direct tumour cell killing
- directly bind to cancerous cell
- interfere with growth pathway, block signalling
- trigger apoptosis
2. immune-mediated tumour cell killing
- identify cancer cells as foreign so that immune cells destroy them opsonisation)
- trigger cytotoxic T cells (or NK cells) to destroy them
- can be combined with radioactive particles and chemotherapy drugs to deliver them directly to cancer cell (so that drugs do not harm other cells like in normal chemotherapy- advantage: fewer side effects, less chemotherapy required)
3. vascular and stromal cell ablation
- prevent cell growth by blocking molecules that attract new blood vessels to cancer cells (stops blood flow so cells cannot get nutrients)
- block cancer cells from receiving growth factor signals
For immune diseases:
- block certain steps, target cell types to switch off to suppress overactive immune system
89
what is multiple sclerosis?
- immune cells attack the central nervous system
- specifically the myelin sheath around nerve cells
Biology 3/4
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