Immunity (4) Flashcards

1
Q

what do phagocytes do after phagocytosis

A

They produce cytokines; which act as cell-signalling molecules, informing other phagocytes of the infection; stimulates them to site of inflammation/infection.

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2
Q

name two viral pathogens + two bacterial pathogens in animals

A

virus: HIV and INFLUENZA
bacterial: TUBERCULOSIS and BACTERIAL MENINGITIS ​

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3
Q

what occurs when the skin is cut

((two parts))

A

Blood clots rapidly to seal a wound and prevent entry of pathogens. POSITIVE FEEDBACK: clotting cascade.

The clot dries out forming a hard scab.

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4
Q

what is an autoimmune disease

+ 5 examples

A

When the body’s own cells become antigens (self-antigens). Tf the body’s immune system attacks its own cells.

  • Rheumatoid arthritis- synovial fluid + membranes of joints attacked*
  • Multiple sclerosis- myelin sheath of nerve axons attacked*
  • Lupus- many tissues attacked*
  • Diabetes Type 1*
  • Eczema*
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5
Q

A graft of tissue, such as skin, from a different person is usually rejected by the body. Which immune system cells cause this

A

The graft is rejected by T-lymphocytes because they circulate in the blood and can gather at the graft site.

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6
Q

why is the is the second exposure to an antigen much larger than during a vaccination/first exposure

A

The vaccination/first exposure is the primary exposure, which takes time because the immune system goes through clonal selection, clonal expansion/proliferation and differentiation.

The second exposure already has long-lasting memory cells from the first infection, meaning there is a more rapid and larger response as the memory cells act as cell-signalling molecules.

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7
Q

function of immunoglobulins?

A

Identify and neutralise foreign material, eg. b**acteria & viruses.

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8
Q

how are ringworm + athlete’s foot transmitted and what are their symptoms

A

DIRECT (AF: skin to skin, R: housing and bedding) & INDIRECT

AF: itchiness, R: inflammation, scaly patches, itchiness

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9
Q

how is a new vaccine created against a new strain of influenza virus

A

WHO + CDC laboratories collect samples of different strains, and test the effectiveness of different influenza vaccines against them. Each year the most effective is chosen, so governments/health authorities implement a programme of vaccination.

Some people can be given a vaccine to prevent the strain causing an epidemic in another country & spreading globally.

The antigen is either inactive/dead/attenuated.

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10
Q

describe the second exposure to an antigen/pathogen

A
  • Memory cells replicate rapidly on encountering the antigen
  • Response is much greater- more rapid elimination of Ag/Pg
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11
Q

how do phagocytes (macrophages, neutrophils + dendritic cells) pass from the blood into the tissue fluid

A
  1. Lobed/narrow nucleus
  2. They can squeeze between pores/gaps/fenestrations in the capillary walls/endothelium
  3. Cells can change shape
  4. Histamines from mast cells make the capillary walls/endothelium leaky
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12
Q

how do the following actively defend plants from pathogens:

  • Hypersensitivity*
  • Systemic Acquired Resistance*
  • General toxins*
A

Hypersensitivity- immediate death of tissues surrounding the site of infection by a pathogen

SAR: signalling molecule travels to uninfected areas + gives protection.

Toxins- plant produces chemicals that when broken down, produce a toxic product eg. cyanide

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13
Q

what are immunoglobulins secreted from and where are they secreted into

A

By B lymphocytes (B cells) into the blood.

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14
Q

why are personalised medicines necessary?

A

Genes determine how the body responds to certain drugs- making them more or less effective for different people.

Personalised drugs are tailored to an individual’s DNA; genetic information is used to predict how a person will respond; the most effective drug will be prescribed.

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15
Q

how is black sigatoka transmitted + its symptoms?

A

INDIRECT transmission eg. wind, rain, water, irrigation

large brown patches

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16
Q

how are HIV & influenza transmitted and what are their symptoms

A

HIV = direct transmission eg. bodily fluids

depressed immune system, AIDS

influenza = indirect transmission by droplet infection

runny nose, fever, coughing, sneezing

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17
Q

name the 5 passive physical barriers present in plants all the time

+ what is the difference between animal/plant disease defence

A

-waxy cuticle

-bark

-cellulose cell walls

-casparian strip

-closing stomata

Plants do not heal diseased tissue, they seal it off & discard it.

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18
Q

which ROUTINE VACCINES are offered to everybody in the UK

A

MMR- measles, mumps, rubella- attenuated virus given

Meningitis C- bacterial

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19
Q

what is IMMUNITY (3 marks)

A

The ability of an organism to resist a particular infection or toxin by the action of specific antibodies and sensitised white blood cells. Either:

NATURAL- produced by own antibodies or from antibodies mother-foetus/newborn

ARTIFICIAL- administrated medically

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20
Q

Define autoimmune disease (2 marks)

A

A disease in which the body produces antibodies that attack its own tissues, leading to the deterioration and sometimes destruction of such tissue.

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21
Q

how is bacterial meningitis transmitted and what are the symptoms

A

DIRECT + INDIRECT transmission eg. kissing, coughing, sneezing, (respiratory secretions)

Symptons = fever, headache, neck stiffness, light sensitivity

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22
Q

what is the specific/adaptive immune response

A

A pathogen and antigen-specific immune response with both cell-mediated and humoral components. Characterised by immunological memory.

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23
Q

name the parasite that causes malaria + the vector for the malarial parasite

A

Plasmodium is the parasite eg. Plasmodium vivax**, Plasmodium malariae etc.

female Anopheles is the vector

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24
Q

how is tobacco mosaic virus transmitted and what are the symptoms

A
  • DIRECT transmission: contact between plants*
  • INDIRECT transmission: farm machinery, tobacco products*

Yellow streaking, stunted growth.

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25
Q

name a bacterial pathogen in plants + what are the symptoms

A

(bacterial plant infection)

RINGROT in potatoes

discolouration, oozing, wilting leaves

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26
Q

define an OPSONIN

A

Any substance that binds to foreign microorganisms or cells, making them more susceptible to phagocytosis.

They act as cell-signalling molecules.

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27
Q

why do some vaccines have to be changed every year?

A

The antigens on the CSM change regularly eg. the influenza virus, forming new strains.

Therefore the memory cells from one vaccination with one strain will not recognise the new strain with different antigens; strains are immunologically different.

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28
Q

why is there a HINGE REGION on an immunoglobulin

A

to allow movement of variable regions, therefore increasing antigen-binding potential

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29
Q

which cells carry out PHAGOCYTOSIS

A

Specialised phagocytic white cells i.e. phagocytes- neutrophils, macrophages + dendritic cells.

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30
Q

differences between types of immunity- active + passive

Exposure?

Time/how rapid?

How long protection will last?

Memory cells produced?

A

ACTIVE

REQUIRES EXPOSURE TO ANTIGEN

TAKES A WHILE FOR PROTECTION TO DEVELOP

LONG-TERM

M CELLS PRODUCED

  • passive*
  • no exposure to antigen*
  • protection is immediate*
  • short-term*
  • m cells are not produced*
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31
Q

what happens in an inflammatory response after the mast cell histamines make capillary walls leaky

A

Fluid, platelets & antimicrobial proteins enter tissue from the capillary. Clotting begins.

Further cytokines secreted by mutliple cells- attract phagocytes from blood.

Phagocytosis by neutrophils + macrophages of pathogens and cell debris at the site.

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32
Q

why does the government aim to vaccinate a large % of the population

A

Herd immunity- helps to prevent epidemics i.e. mass outbreaks of disease.

-Those not vaccinated are unlikely to become infected because they will not come into contact with anyone who has the disease.

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33
Q

what is the SPECIFIC immune reponse

A
  • Recognises & targets a specific antigen only
  • Involves lymphocytes (specialised leucocytes), which are produced in the bone marrow and differentiate in the bone marrow; B lymphocytes + thymus: T lymphocytes
  • Interleukins/cytokines.
  • Humoral + Cell-mediated parts.
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34
Q

what are the types of transmission & the 5 factors affecting transmission of communicable disease in plants

A

DIRECT transmission - eg. touching

INDIRECT TRANSMISSION - wind, water, soil, animals, humans

  1. poor _____ nutrition
  2. susceptibility to disease
  3. over-crowding
  4. abiotic conditions
  5. climate change
35
Q

what is ACTIVE immunity

A

An organism’s own memory cells are produced and antibodies are obtained from organism’s own B cells.

i.e. the immune system has been stimulated by an antigen

36
Q

what is the inflammatory reponse

A

A localised response to pathogens/irittants/damage resulting in inflammation at the site of the wound i.e. heat, pain, swelling/oedema, redness.

The heat prevents pathogens reproducing.

37
Q

what is the difference between a primary and secondary immune response?

A

PR: The response of the immune system the first time it is exposed to an antigen.

SR: The response of the immune system the second and subsequent times it is exposed to an antigen.

38
Q

How do antibodies act as ANTI-TOXINS

A

They combine with toxins secreted by bacteria to render them harmless

eg. Tetanus + Diphtheria toxins

39
Q

what kind of protein is an immunoglobulin

how many antigens can an antibody bind to

A
  • Y-shaped GLOBULAR protein*
  • two antigen molecules per antibody*
40
Q

explain how production of callose, tyloses + phtoalexins help actively defend the plant from pathogens

A

CALLOSE- Closes plasmodesmata, blocking passage between cytoplasms to inhibit pathogen entry. Deposited in sieve pores to block transport of phloem sap to entire plant.

TYLOSES- ingrowths in xylem vessels. (blocks xylem lumen)

PHYTOALEXINS- cell-signalling molecules produced as a response to breakdown products of cellulose by bacteria + fungal cellulases. They stimulate production of chitinase enzymes to digest fungi cell wall. Disrupt cell membrane & delay reproduction of bacteria.

41
Q

in which natural compounds are many medicinal drugs found?

give 3 examples

A

Plants, animals, microorganisms (only a small proportion have been investigated)

  • Penicillin obtained from fungus*
  • Some cancer drugs made using soil bacteria*
  • Alzheimer’s disease drugs produced from daffodils*
42
Q

what is natural active immunity

A

EXPOSURE TO A DISEASE: immune system makes its own antibodies + memory cells

43
Q

what is immunisation and vaccination

A

A programme that can involve both artificial active immunity & artificial passive immunity

Artificial active immunity only.

44
Q

what is immunological memory

A

The ability of the immune system to respond rapidly in the future to antigens encountered in the past.

45
Q

name the human cells in which the malaria parasite reproduces

A

Hepatocytes + erythrocytes

46
Q

WHAT ARE ANTIBIOTICS FOR

A

Chemicals that kill or inhibit the growth of bacteria.

Used in drugs to treat bacterial infections- do not harm human body cells or viral cells because they do not have a cell wall, unlike bacteria (peptidoglycan).

The antigen is either inactive/dead/attenuated.

47
Q

What causes the measles vaccine to be less effective in children from less economically developed countries?

A

Their diet it protein deficient

48
Q

what happens in the first exposure to a pathogen

A

CLONAL SELECTION

Clones of lymphocytes that are complementary bind to antigens, all other lymphocytes are blind

CLONAL EXPANSION/PROLIFERATION

Those that are complementary increase in number- plasma cells.

CLONAL DIFFERENTIATION

Some clones differentiate into memory cells.

49
Q

what is artificial active immunity

A

Immune system produces own antibodies and memory cells after exposure to a vaccine.

50
Q

what is natural passive immunity

A

Antibodies are provided by natural means, i.e. from the placenta or breast milk.

from mother to baby

51
Q

what are interleukins

A

A group of cytokines (cell-signalling proteins + other signal molecules) secreted by leucocytes and regulate proliferation, differentiation & activation of the cells of the specific immune system.

52
Q

name two potential problems with antibiotics

A

Side effects/severe allergic reactions in some people.

Antibiotic resistance.

53
Q

name a protoctista + a fungal pathogen in plants

A

PROCTISTA = blight (in tomatoes, potatoes etc.)

FUNGAL = black sigatoka eg. in bananas

54
Q

how is malaria transmitted + what are the symptoms

A

by a vector i.e. Plasmodium, in a mosquito

tiredness, fever, decreased O2, death

55
Q

Outline ANTIBIOTIC RESISTANCE

A
  • genetic resistance in a population
  • natural resistance
  • antibiotic kills all
  • resistant survive
  • lack of competition = thrive
  • allele passed for resistance passed on (artificial selection)
  • resistant spreads, (frequency)
  • ‘superbugs’ antibiotic redundant
56
Q

why are booster vaccines given

A

to make sure memory cells are produced (after several years)

57
Q

what is clonal selection

A

A model for how B and T cells are selected to target specific antigens invading the host.

58
Q

Define PHARMING + Nanotechnology in synthesis of medicines

A

Using animals to mass-grow drugs/make many copies.

Particles** used to **deliver drugs** to **pathogens or tumours.

59
Q

give 5 examples of primary physical+chemical defences

A
  1. Nasal cavity- hairs & mucus trap microorganisms, the mucus is wafted away or digested. Other MUCOUS MEMBRANES- urethra, lungs, vagina, alimentary canal
  2. Tear glands- clean eyes with tear solution containing lysozyme
  3. Skin- Impervious unless broken, friendly bacteria outcompete, sebum + fatty acid secretions kill many bacteria
  4. Stomach- Acidic juices kill many bacteria
  5. Large intestine- bacteria outcompete pathogenic bacteria
60
Q

name 2 ways in which the body forcibly removes pathogens

A

EXPULSIVE REFLEXES

Coughing + sneezing.

Caused by pathogens in the linings of the airways eg. in the mucus in the upper respiratory tract.

61
Q

what is cell-mediated immunity

A

An immune response involving the activation of macrophages, specific T cells + cytokines against antigens.

62
Q

Describe the structure of an antibody

A

4 polypeptide chains: two heavy two light

The heavy chains are held at a HINGE REGION by INTERCHAIN DISULFIDE BONDS

The phagocyte binds to the constant region, whilst the variable region binds to the specific complementary antigens on a pathogen via the antigen-binding site.

63
Q

what is an ANTIGEN

A

An identifying chemical on the surface of a cell or macromolecule that induces an immune response.

eg. allergens, pathogens & foreign bodies i.e. non-self antigens.

64
Q

name two fungal pathogen + a protoctista pathogen in animals

A

ATHLETE’s FOOT and RINGWORM

MALARIA from PLASMODIUM

65
Q

explain how antibodies act as AGGLUTININS

A

Antibodies bind to two identical antigens or two or more pathogens, causing them to CLUMP together

-tf difficult for them to spread/easy for phagocytes to engulf them

66
Q

what is the difference between Innate and Acquired immunity

A

INNATE immunity: non-specific rapid response to a range of pathogens

primary defences- prevent entry of pathogen into body

secondary defences- internal, killing pathogen when it has entered system

ACQUIRED immunity: specific immune response, targeted at one particular pathogen

67
Q

briefly describe the SPECIFIC/ADAPTIVE immune response

A

humoral

B cells activated by T cells

B cells secrete antibodies into the blood plasma, they bind to antigens.

cell-mediated

Helper T cells bind to an APC eg. macrophage, and are activated

Helper T cells divide/proliferate

Helper T cells activate B cells, cytotoxic T cells & produce T memory cells

Cytotoxic T cells destroy infected body cells

68
Q

name 6 active defence mechanisms in plants

A
  1. HYPERSENSITIVITY (immediate death of tissues)
  2. production of CALLOSE (closes plasmodesmata)
  3. production of TYLOSES (xylem vessel blockages)
  4. production of PHYTOALEXINS cell-signalling molecules
  5. Systemic Acquired Resistance cell-signalling molecules
  6. General toxins
69
Q

how does the skin/wound heal after a scab has formed

A

Epithelial cells below the scab start to grow, sealing the wound permanently. damaged capillaries regrow

Collagen fibres are deposited to give new tissue strength.

Scab falls off once epidermis normal and wound is healed.

70
Q

Describe the stages of the clotting mechanism

A

Platelets gather near the wound and release clotting factors, stimulating the conversion of prothrombin to thrombin, which splits fibrinogen to form fibrin.

FIBRIN FIBRES form a mesh over the wound, trapping RBCs + platelets- stopping the bleeding.

Clot hardens-scab- new cells grow for repair- enzyme plasmin released to dissolve clot.

71
Q

name the 5 PASSIVE chemical defence mechanisms in plants

A
  • secretion of toxins
  • secretion of enzyme inhibitors
  • sticky resin in bark
  • secretion of growth substance, promoting growth of microorganisms that compete with the pathogen
  • receptors on cell surface detecting pathogen, activate plant defences
72
Q

explain how antibodies act as OPSONINS

A

The antibodies cover the pathogen(s) to facilitate phagocytosis bc the phagocytes can bind to their constant regions (receptors).

By attaching to bacteria, they mark the pathogen for phagocytes.

If binding to viruses, they prevent the virus binding to a host.

73
Q

what is tobacco mosaic virus

A

A viral pathogen in plants.

74
Q

what is the function of a vaccine

A

They contain antigens (free or attached to a dead or weakened pathogen) so that the body produces memory cells against a particular pathogen- without the pathogen causing disease/symptons of it.

Vaccination causes immunisation, i.e. the process by which you develop immunity.

75
Q

PASSIVE immunity?

A

Antibodies are not produced by organism’s own B cells, but obtained otherwise.

Memory cells not produced.

76
Q

how is tuberculosis transmitted and what are the symptoms

A

INDIRECT transmission by droplet infection

-causes a respiratory disorder

77
Q

Describe the process by which a pathogen is destroyed once recognised

A

PHAGOCYTOSIS of pathogen/foreign cell

  1. Endocytosis of pathogen, enabled by cytoskeleton, forming pseudopodia.
  2. This forms a phagosome, which is a vacuole containing bacteria.
  3. Phagosome fuses with a lysosome, which contains hydrolytic enzymes, forming a phagolysosome.
  4. These begin to hydrolyse the pathogen into monomers eg. amino acids, fatty acids.
  5. The antigens of the pathogen are presented on the surface of the phagocyte- becomes an APC.
  6. Waste products released by exocytosis.
78
Q

After CLONAL SELECTION, what happens to the clones and what are their roles

A

expansion/proliferation

they differentiate into PLASMA CELLS; carry out cell function, secreting antibodies

and MEMORY CELLS; they have a long life-span, replicate occassionally and induce a rapid second immune response and the proliferation of many plasma cells

79
Q

how is synthetic biology used in antibiotic production

A
  • Technology is used to design/produce artificial proteins, cells + microorganisms
  • eg. engineering bacteria to destroy cancer cells while leaving healthy body cells intact
80
Q

what are the 3 types of T cell + their functions

A

T helper cell : receptors on surface membrane bind to APC. T cells produce interleukins that stimulate proliferation of B cells & all T cells.

T killer/cytotoxic cell

T regulator

81
Q

what is the function of MACROPHAGES + MAST CELLS when the body is wounded eg. skin broken

A

MACROPHAGES RELEASE CYTOKINES - cell-signalling molecules- alerting other phagocytes to the pathogen(s) in the site of infection.

MAST CELLS RELEASE HISTAMINES - type of cytokine- making nearby capillary walls leaky (for phagocytes).

82
Q

what is artificial PASSIVE immunity

A

Antibodies injected into bloodstream

83
Q

how is blight transmitted and what are the symptoms

A

INDIRECT transmission eg. spores in the wind

rotting flesh, foul smelling

84
Q

what are the factors that increase the chance of infection of tuberculosis

A
  • not vaccinated against TB
  • weakened immune system
  • overcrowding
  • poor ventilation of housing
  • homelessness
  • lifestyle- poor diet/ lack of protein/ malnourished/smoking/alcoholism
  • close/prolonged contact with infected individuals
  • close contact with people from/visiting, area where TB is common
  • consumption of milk/beef from infected cattle/in developing countries