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Biology CAP 3 > Immunology > Flashcards

Immunology Flashcards

1
Q

State two ways pathogens cause harm

A

Viruses destroy cells by replicating inside the host
Bacteria produce toxins

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2
Q

Harm causing cells

A

Pathogens
Cells from other organisms of the same species
Abnormal body cells - cancer cells
Toxins secreted by pathogenic bacteria - snake venom

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3
Q

Antigen

A

Molecule (protein) that stimulates an immune response
Results in the production of a specific antibody
Antibody generator

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4
Q

Non self cells

A

Foreign cells or pathogens
Covered in specifically shaped antigens
Initiates an immune response to destroy the cell/pathogen

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5
Q

Phagocytes

A

White blood cells
Will engulf and digest non self cells

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6
Q

Phagocytosis

A

The processor engulfing and digesting a non self cell/pathogen

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7
Q

First line of defence

A

Tears
Mucus/Cilia
Skin
Scabs
Phagocytes
Eyelashes

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8
Q

Describe the process of non specific immunity

A
  1. Pathogen is engulfed by phagocyte
  2. Engulfed pathogen enters cytoplasm in a vesicle and his now a phagosome
  3. Lysosomes fuse with phagosome releasing hydrolytic digestive enzymes
  4. Lysosome enzymes hydrolyse the pathogen
  5. Waste materials released by exocytosis
  6. Antigens presented on the cell surface and phagocyte becomes an antigen presenting cell
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9
Q

Specific immunity

A

A specific response to a specific antigen on the surface of a cell that is non self

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10
Q

What it the primary response

A

Cell mediated immunity using T lymphocytes

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11
Q

Cellular response

A
  1. Phagocyte engulfs and hydrolyses the pathogen and presents the antigen on its cell surface
  2. T Helper cell with specific receptor molecule binds to presented antigen
  3. Once T Helper cell binds to activated antigen, it is activated
  4. T helper cell clones rapidly by mitosis
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12
Q

What is the advantage of having more T Helper cells

A

More cytokines to attract phagocytes to the area of infection

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13
Q

Role of T Helper cells

A
  1. Specific T Helper cells bind to antigen presenting cell
  2. Release cytokines that attract phagocytes to the area of infection
  3. Release cytokines that activate cytotoxic killer T cells
  4. Activates specific complimentary B cells
  5. Forms memory cells
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14
Q

Role of cytotoxic killer T cells

A

Locate and destroy infected body cells that present the correct antigen
2. Binds to the antigen presenting cell
3. Release perforin protein which creates holes in the membrane of the cell to destroy the APC

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15
Q

Humoral response

A

Involves the activation of B cells to produce antibodies. B cells are stimulated by the release of cytokines

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16
Q

B cell activation

A

A specific T helper cell with correct receptor binds to presented antigen and locates and activates specific complimentary B cell
The cytokine releases chemicals that signal the B cells to clone by mitosis
The B cells differentiate into plasma cells or memory cells.
Plasma cells - produce and secrete specific antibodies into the blood plasma
Memory cells - Remain in the body to rapidly reproduce in the case of pathogen re entering

17
Q

Antibody

A

Protein made in response to foreign antigen

18
Q

Antibodies structure

A

Quaternary structure
Four polypeptide chains
Y shaped
Antigen binding sites on top of the Y
Main body called constant region
Variable regions have different tertiary structure
Complimentary to one antigen
Disulphide bridges hold chains together

19
Q

Antigen + antibody =

A

ANtigen - antibody complex

20
Q

How do antibodies assist in the destruction of pathogens

A

Agglutination - when antibodies bind to antigens and clumps together
Opsonisation - marking pathogens so phagocytes recognise and destroy there pathogen more effectively
Lysis - bind to antigens, leading to the destruction of pathogens membrane
Anti-toxin - binds to toxins to prevent the molecules from binding to their complimentary receptors
Prevent pathogen replication

21
Q

Memory cells

A

Not directly related to destroying the pathogen
Activated by cytotoxic killer T cells
Divide rapidly by mitosis
Secondary response

22
Q

Secondary response

A

Rapid and extensive

23
Q

Antigenic variability

A

The change in the antigen due to mutation
Makes it difficult to vaccinate against these pathogens

24
Q

Passive immunity

A

No exposure to antigen
No production of memory cells
By mother or injection of antibodies

25
Q

Active immunity

A

Exposure to antigens
Provided by memory cells after a primary response

26
Q

Vaccination definition

A

A dead, weakened or attenuated form of the pathogen

27
Q

Role of vaccine

A

Pathogen engulfed by phagocyte and becomes antigen presenting
Specific T helper cell binds to antigen
T helper cell stimulates a B cell by releasing cytokines
B cells divide by mitosis
Plasma cells produce antibodies
Memory cells remember antigen

28
Q

Herd immunity

A

If over 85% of the population are vaccinated there is little chance of the disease spreading

29
Q

Vaccine disparity

A

Availability to get value by economic status eg have enough money to buy PPE and vaccines for country

30
Q

Ethical issues related to vaccines

A

Developmental - animal testing?
Human testing - who should be tested?
Is it available to everyone
Balancing risks and benefits
Compulsory?
Should we be aiming to eliminate an organism - mosquitos to kill malaria?

31
Q

Uses of monoclonal antibodies

A

Research
Immune assays - pregnancy tests
Diagnosis
Targeting drugs
Killing specific cells
Isolating specific chemicals

32
Q

ELISA test

A

Monoclonal antibodies fixed to the surface of the test well
Sample containing molecule to be detected binds to anybody due to complementary shape
Second monoclonal antibodies (with enzyme) added and binds to molecule
Washed so unbound antibodies are washed away
Substrate added - chemical colour change visible
Colour change = positive result

33
Q

Virion

A

Infections virus particle that enters a host cell and multiplies

34
Q

HIV

A

Human immunodeficiency virus

35
Q

HIV structure

A

HIV capsid - core of HIV RNA
HIV envelope - outer surface
HIV enzymes - proteins that carry out steps in the HIV life cycle
HIV glycoproteins - spikes embedded into the envelope
RNA - genetic material

Biology CAP 3 (4 decks)

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