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Biology A level AQA > Chapter 5 - Cell recognition and the immune system > Flashcards

Chapter 5 - Cell recognition and the immune system Flashcards

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1
Q

two lymphocyte responses?

A
  • cell-mediated (T-lymphocytes)

- humoural responses (B-lymphocytes)

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2
Q

definition of a pathogen?

A

any foreign body/microorganism that causes disease

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3
Q

how are pathogens identified as non self?

A

specific molecules on cell surface membrane

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4
Q

what molecules would be identified by the body? (4)

A
  • pathogens e.g. viruses
  • cells from other organisms
  • toxins
  • abnormal body cells e.g. cancers
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5
Q

how do lymphocytes recognise own cells in adults? (3)

A
  • lymphocytes produced in bone marrow only encounter self antigens
  • any lymphocytes which show an immune response towards self-antigens undergo apoptocis
  • no clones of anti-self lymphocytes appear in blood
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6
Q

how do lymphocytes recognise own cells in a fetus?(1)

A
  • anti self lymphocytes die or are suppressed
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7
Q

outline phagocytosis (5)

A
  • Phagocyte attracted to pathogen by chemical products along concentration gradient
  • phagocyte receptors bind to antigens on surface of pathogen
  • lysosomes in phagocyte migrate to the phagosome which is forming
  • lysosomes release lysozymes into phagosome, which hydrolyses the pathogen
  • products of hydrolysis are absorbed by phagocyte
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8
Q

definition of an antigen

A

part of an organism/substance that is recognised as non-self by the body to trigger an immune response e.g. cell surface proteins on a pathogen

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9
Q

what are the two types of lymphocyte?

A

B lymphocytes

T lymphocytes

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10
Q

where do the two main types of lymphocyte form/mature?

A

B - in the bone marrow (humoural immunity)

T - in the thymus gland (cell mediated immunity)

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11
Q

How are T-lymphocytes able to recognise invading cells? (4)

A
  • phagocyte present antigens of engulfed pathogens on their surface
  • or cells invaded by a virus present antigens on their surface
  • transplanted cells have different antigens
  • cancer cells have different antigens
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12
Q

Why is it that T-lymphocytes are said to be involved in cell-mediated immunity?

A

they only respond to antigens presented on cells rather than in fluids

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13
Q

outline the response of a T-lymphocyte to the detection of a pathogen (4)

A
  • phagocyte engulfs pathogen and presents antigens on its surface
  • receptors on specific T helper cells fit exactly onto these antigens
  • attachment prompts T cell to divide rapidly by mitosis
  • these daughter cells; stimulate phagocytes to carry out phagocytosis, stimulate B-cells to divide and produce antibodies - develop into memory cells, activate cytotoxic T cells.
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14
Q

How do cytotoxic T cells kill infected cells? (3)

A
  • produce protein called perforin
  • this makes many holes in the CSM
  • cell becomes freely permeable to everything and dies
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15
Q

What are antibodies?

A

specific protein produced by B cells in response to the presence of the appropriate antigen

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16
Q

outline the process of humoural immunity by B-lymphocytes (4)

A
  • B-cell with complimentary antibody attaches to antigen
  • antigen enters by endocytosis and is presented on cell surface
  • T helper cells bind to processed antigens triggering B cells to divide by mitosis
  • all clones produce same antibody therefore known as monoclonal (variety of monoclonal antibodies used to fight one type of pathogen due to antigenic variability)
17
Q

what do the cells of B cell clones develop into? (2)

A

plasma cells - secrete antibodies directly into blood plasma
memory cells - responsible for secondary immune response, able to divide rapidly

18
Q

how do antibodies assist in the destruction of pathogens? (2)

A
  • cause agglutination, clumps them together making it easier for phagocytes to engulf
  • mark pathogens of phagocytes to engulf
19
Q

What are monoclonal antibodies?

A
  • specific to one antigen

- produced by a single clone

20
Q

outline how monoclonal antibody therapy can be used to treat cancer (3)

A
  • monoclonal antibodies produced specific to antigens of cancer cells
  • antibodies given to patient to attach to cancer
  • stop chemical signals that stimulate uncontrolled growth and replication of cancer
21
Q

why might monoclonal antibody therapy be a better treatment than other cancer treatments e.g. chemo?

A
  • specific to patient

- less side effects, own antibodies

22
Q

give 2 examples of diseases that can be diagnosed using antibody testing

A

influenza
hepititus
chlamydia
prostate cancer

23
Q

how is early pregnancy detected?

A
  • hormone HCG released from placenta in urine

- binds to antibody-colour complex causing a colour change

24
Q

state 3 ethical issues for the use of monoclonal antibodies

A
  • production uses mice who have cancer deliberately induced
  • patients must have informed consent
  • drugs trials are not always safe
25
Q

what is passive immunity? (2)

A
  • introduction of antibodies from outside e.g. antivenom

- not long lasting

26
Q

what is active immunity? (2)

A
  • stimulation of antibody production from own immune system

- natural active immunity, artificial active immunity

27
Q

what is natural active immunity?

A

when an individual is naturally infected with a disease which stimulates an immune response which leaves memory cells

28
Q

what is artificial active immunity?

A

vaccination - purposeful introduction of disease causing an immune response and memory cells

29
Q

what is vaccination?

A

introduction of appropriate disease (or/including antigens) into body to induce artificial immunity

30
Q

what do vaccines aim to produce on the body?

A

immunity to secondary exposure through memory cells

31
Q

state the features of a successful vaccination programme (5)

A
  • economically viable on a large scale
  • few side effects so people aren’t discouraged
  • means of production, storage, transport
  • proper administering equipment e.g. needles
  • possible to vaccinate majority for herd immunity
32
Q

what are the reasons a vaccination might not lead to a disease being eliminated? (6)

A
  • not all become immune, faulty immune systems
  • may develop disease just after vaccination but before immunity
  • pathogen may frequently mutate (antigenic variability)
  • too many strains of pathogen to vaccinate against them all
  • pathogens may hide from immune system
  • people may object to vaccination programs
33
Q

ethics of vaccination? (7)

A
  • production , animals
  • side effects, long term harm
  • informed consent in human testing not totally possible
  • use of countries in which disease is widespread to trial vaccine
  • compulsory vaccination
  • expensive vaccination for almost eradicated diseases
  • individual health risks vs population health
34
Q

how does HIV replicate? (6)

A
  • HIV binds to CD4 on (usually) T helper cells
  • capsid fuses to CSM, RNA and enzymes enter T helper cell
  • HIV reverse transcriptase makes HIV DNA
  • DNA inserted into T helper cell nucleus
  • nucleus the makes mRNA as if it were the cells own DNA
  • HIV breaks way with part of CSM forming its lipid envelope
35
Q

How does HIV cause symptoms of AIDS? (3)

A
  • killing/interferring with normal functions of T helper cells
  • T helper cells not available for cell mediated immunity
  • means no B cells produced of cytotoxic T cells, means the body can’t respond to any infection
36
Q

technique for ELISA test? (7)

A
  • apply sample to surface and allow binding
  • wash away unattached antigens
  • add specific antibody
  • wash away excess antibody after time for binding
  • add second antibody that binds to first one
  • add colourless substrate of enzyme
  • amount of antigen present is relative to the intensity of colour which develops
37
Q

Why do viruses not respond to antibiotics? (2)

A
  • rely on host cells for metabolic activities (antibiotics usually work by disrupting metabolic activities)
  • protein coat rather than murien cell wall means antibiotics can’t break down

Biology A level AQA (19 decks)

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