Cell recognition and the immune system Flashcards

1
Q

types of cells that can stimulate the immune system

A

-pathogens
-cells from other organisms of the same species
-abnormal body cells
-toxins

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2
Q

describe the process of phagocytosis

A

-Receptors on the surface of the phagocyte recognises the antigens on the pathogen and binds to it complementary.

-cytoplasm of the phagocyte change shape to engulf the pathogen.

-phagocyte engulfs the pathogen and forms a phagosomes.

-lysosome fuses with the phagosome and releases lysozymes( digestive enzymes) .

-lysozymes is released into the phagocyte which hydrolyses the pathogen and destroys it.

-phagocyte presents antigens on its surface to activate other immune system cells ( antigen-presenting phagocyte)

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3
Q

state the difference between the non-specific defence mechanism with the specific defence mechanism

A

-non-specific defence mechanism : immediate response , same for all pathogens (phagocytes)

-specific defence mechanism: slower response, specific to each antigen on pathogens (lymphochytes)

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4
Q

what are the examples of non-specific defence mechanism

A

physical barrier: e.g : skin, platelets, hydrochloric acid in stomach,epithelia covered in the mucus and moved by the cilia…

phagocytosis

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5
Q

what are the examples of specific defence mechanism

A

-cell mediated response: T lymphocytes
humoral response : B lymphocytes

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6
Q

where are B and T lymphocytes formed from

A

stem cells in the bone marrow

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7
Q

why are t cell described as ‘cell mediated’

A

-T cells only respond to antigens which are presented on cells (APC) and not antigens detached from cells and within the body fluids e.g : blood

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8
Q

describe the cell mediated response
t-cells

A

1) once pathogen has been engulfed and destroyed by a phagocyte, the antigens are presented on the cell surface- now known as antigen- presenting cell (APC)

2) antigen- presenting cell are complementary to the recpetors of the helper T -cells and binds.

3) Once binded, this activates the helper T cells to divided by mitosis to replicate and make large numbers of clones of helper T-cells

4) cloner helper t cells differentiate into different cells by

-some remain as helper T-cells + activate B lympocytes

-some stimulate cytotoxic t cells ( Killer t-cells) that produce perforin ( pores/holes embeddedin the cell membrane) so that any substances can enter and leave the cell.
-causes cell death

-some stimulate phagocytes to perform more phagocytosis

-some develop into memory cells for that shaped antigen

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9
Q

n1)there are A different B-cells which have surface antibodies that are complementary to B different antigens so the antibodies act as receptors to the antigens

A

A) 10 million
B) 10 million

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10
Q

step of b-cell humoural response

A

1) B cell (antibody) binds to (viral) specific/complementary
receptor/antigen.

2) antigens enter the B cells by endocytosis, B cells process the
antigens and become antigen presenting B cells

3) helper T cells bind to the antigen presenting B cells which activate rapid cell division by mitosis to form cloned B cells

4 cloned B cells differentiate into plasma cells or memory B cells

  • plasma cells produces anitbodies fast and in large numbers
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11
Q

Describe and explain the role of antibodies in stimulating phagocytosis.
Do not include details about the process of phagocytosis

A
  • are markers
    -(Antibodies) cause agglutination
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12
Q

describe the difference between active immunity and passive immunity

A

1) Active involves memory cells whilst passive doesn’t

2) Active involves the production of antibody by plasma cells/ memory cells

3) Passive involves antibody introduced into the body from the outside

4) passive is short term because antibody is broken

5) Active can take time to develop

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13
Q

define herd immunity

A

when the vaccination of a significant proportion (~ 80%) of the population provided protection for individuals who have no developed immunity.

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14
Q

what is antigen variability

A

-Pathogens can mutate frequently. if a mutation occurs in the gene which codes for the antigen ,then the shape of the antigen changes

  • Any previous immunity to this pathogen is no longer effective as all the memory cells in the blood will have memory of the old antigen shape
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15
Q

describe how HIV is replicated

A

1) attachment proteins attach to receptors on helper T-cells

2) nucleic acid enters the cell

3) Reverse transcriptase converts RNA to DNA

4) Viral protein is produced

5) virus assembled and and released from the cell.

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16
Q

ADCs are molecules made of a monoclonal antibody linked to a cancer
drug.
Figure 1 shows how an ADC enters and kills a tumour cell.
The process of entering the cell and the breakdown of the antibody to
release the drug is very similar to phagocytosis.

Use your knowledge of phagocytosis to describe how an ADC enters and
kills the tumour cell. (3)

A

1) cell engulfs the antibody the ADC

2) lysosome fuses with the phagosome

3) lysozyme break down the antibody

17
Q

Describe how the human immunodeficiency virus (HIV) is replicated once
inside helper T cells (TH cells).

A

1) RNA is converted into DNA using reverse transcriptase

2) DNA is inserted into the helper t cells

3) DNA is transcribed HIV mRNA

4) HIV mRNA is translated into

18
Q

What is a monoclonal antibody?

A

-(Antibodies with the) same tertiary structure

19
Q

Give one example of using monoclonal antibodies in a medical treatment.

A
  • block antigens on the cells
20
Q

Describe the role of antibodies in producing a positive result in an ELISA
test.

A

1) antibody binds complementary to antigen;

  1. antibody with enzyme attached is added;
  2. the second antibody is attached to the first antibody
  3. (Substrate added) and colour changes;
21
Q

When a person is bitten by a venomous snake, the snake injects a toxin
into the person. Antivenom is injected as treatment. Antivenom contains
antibodies against the snake toxin. This treatment is an example of passive
immunity.
Explain how the treatment with antivenom works and why it is essential to
use passive immunity, rather than active immunity.

A

antibodies bind to the
toxin and (causes) its destruction;

Active immunity would be slower than passive immunity

22
Q

During vaccination, each animal is initially injected with a small volume of
venom. Two weeks later, it is injected with a larger volume of venom.
Use your knowledge of the humoral immune response to explain this
vaccination programme

A

B cells specific to the venom reproduce by mitosis;

B cells produce) plasma cells and memory cells;

The first dose must be small so the animal is not killed;

23
Q

define antigen

A

foreign proteins
stimulate an immune response

24
Q

define antibody

A

protein
produced by B cells

25
Q

When a vaccine is given to a person, it leads to the production of
antibodies against a disease-causing organism. Describe how.

A
  1. Vaccine contains antigen from pathogen;
  2. Macrophage presents antigen on its surface;
  3. T cell with complementary receptor protein binds to antigen;
  4. T cell stimulates B cell;
  5. B cell secretes large amounts of antibody;
  6. B cell divides to form clone all producing same antibody.
26
Q

Antibiotics are not effective against viruses because:

A

-Viruses do not have a cell wall like bacteria
(murein / peptidoglycan / glycoprotein)

-Viruses do not have metabolic processes / do not replicate / do not make protein

-Viruses do not have do not have enzymes

27
Q

suggest some ethical issues surrounding the use of monoclonal antibodies

A

-production involves animals

drug trials against arthritis + leukaemia resulted in multiple organ failure