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
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2
Q

each type of cell has … on its plasma cell-surface membrane that identify it

A

specific molecules

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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)
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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)

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5
Q

own cells =

A

SELF

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6
Q

foreign cells / pathogens =

A

NON SELF

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7
Q

the surface of all own cells (self) and foreign cells / pathogens (non self) are covered in…

A

specifically shaped antigens

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8
Q

these antigens help identify…

A

each particular type of cell to the host organism

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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.

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10
Q

examples of antigens

A

glycoproteins and glycolipids

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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

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12
Q

the process phagocytes undergo is called

A

phagocytosis

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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)
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14
Q

is phagocytosis specific or non-specific

A

non-specific (works the same for any pathogen that displays a non-self antigen)

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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
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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)
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17
Q

2 stages in response of T lymphocytes (cell-mediated immunity -> primary response)

A
  • antigen presenting
  • clonal selection
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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
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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
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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
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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
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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
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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.

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24
Q

stages in the process: activation of B cells (humoral response -> primary response)

A
  • B cell activation
  • (B cell differentiation)
25
Q

B cell activation process in activation of B cells (humoral response -> primary response)

A
  • 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
Q

what 2 types of cell do B cells differentiate into

A
  • plasma cells
  • memory B cells
27
Q

role of the plasma cells

A

produce and secrete vast quantities of specific antibodies into the blood plasma

28
Q

role of the memory B cells

A

remain in the body to respond to pathogen rapidly ad extensively should there be a future re-infection

29
Q

antibody definition

A

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
Q

structure of the antibodies

A
  • complex proteins
  • quaternary structure
  • 4 polypeptide chains
31
Q

shape of the antibodies

A

‘Y shaped’

32
Q

what is the main part of the antibodies called that is the same in all antibodies

A

constant region

33
Q

what is different in all the antibodies

A

variable region

34
Q

structure of the variable regions

A
  • different primary structure
  • different tertiary structure
  • different shapes
35
Q

what characteristic of the variable region causes the antibodies to be specific

A
  • specific binding site (different for each antibody)
  • therefore specific antibodies are only complementary to 1 antigen
36
Q

when specific antibodies bind to specific antigens due to having specific binding sites, what do they form

A

(permenent) antigen-antibody complex

37
Q

role of the antibodies in destruction of pathogens

A
  • agglutination
  • opsonisation
  • lysis
  • anti-toxin + anti-venom
  • prevent pathogen replication
38
Q

agglutination meaning

A

specific antibodies bind to the antigens on pathogen clump them together

39
Q

opsonisation meaning

A

marking pathogens so phagocytes recognise and destroy the pathogen more efficiently

40
Q

lysis meaning (anitgens)

A

bind to antigens and lead to destruction of the pathogen’s membrane

41
Q

anti-toxin + anti-venom meaning

A

bind to toxins or venom (both usually proteins) to prevent these molecules from binding to their complementary target receptors

42
Q

are memory B cells involved directly in destroying the invading pathogen

A

no

43
Q

process that memory B cells undergo when they encounter the antigen again

A
  • 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
Q

secondary response meaning

A

the activation of memory cells to produce antibodies

45
Q

the secondary response is both…

A

rapid and extensive

46
Q

in the secondary response, the antigen is normally…

A

eliminated before it can cause disease or any symptoms to develop

47
Q

key point to remember in a secondary response

A

more antibodies are produced more rapidly

48
Q

is the immune response more effective or less effective

A

more effective

49
Q

why is the immune response more effective

A

most pathogens have the same antigens on their surface, and so are recognised by memory cells when re-infection occurs

50
Q

why might an individual not be able to initiate a secondary response

A

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
Q

what is a change in an antigen called

A

antigenic variability (drift)

52
Q

what does antigenic variability mean when developing vaccines

A

makes it difficult to develop vaccines against these pathogens

53
Q

what are the 2 ways in which immunity can be gained

A

passive immunity and active immunity

54
Q

characteristics of passive immunity

A
  • no exposure to antigen
  • antibodies are given (mother, antiserum)
  • no memory cells are produced
  • short term
  • fast acting
55
Q

characteristics of active immunity

A
  • exposure to antigen
  • antibodies are produced
  • memory cells produced
  • long term
  • takes time to develop
56
Q

what do vaccines contain

A

antigens from dead, weakened or attenuated pathogens

57
Q

process of a vaccination

A
  • 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
Q

vaccines are not effective against what

A

pathogens which show antigenic variability