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Biology > Cells & Immunology > Flashcards

Cells & Immunology Flashcards

1
Q

Antigen definition

A

a molecule (protein) that stimulates an immune response that results in the production of a specific antibody

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2
Q

Give two types of cell, other than pathogens, that can stimulate an immune response.

A
  1. Cells from other organisms
  2. Abnormal cells
  3. Cells infected by virus
  4. Pathogens
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3
Q

How does an antigen work?

A

The surface of all own cells (self) and foreign cells or pathogens (non self) are covered in specifically shaped antigens. These antigens help identify each particular type of cell to the host organism.

Therefore, if the antigens are not recognised, 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.
- Glycoproteins & Glycolipids are both examples of antigens.

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4
Q

What is a phagocyte?

A

groups of white blood cells which are capable of distinguishing between cells which do or do not display the correct antigens

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5
Q

Phagocytosis

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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6
Q

Why is phagocytosis not always efficient?

A

would take far too long to destroy all the invading pathogens in the event of an infection, which may result in damage to tissues and organs. As a result we also have more efficient systems which involve specific immunity.

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7
Q

Non specific Vs Specific

A

Non specific:
-physical barrier (skin)
-phagocytosis

Specific:
-cell mediated response (T-lymphocytes)
-humoral response (B-lymphocytes)

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8
Q

Describe and explain the role of antibodies in stimulating phagocytosis.

A
  • Bind to antigen
  • Attract phagocytes
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9
Q

What is the cellular response?

A
  1. Phagocyte engulfs & hydrolyses the pathogen, and presents the antigen on the cell surface membrane
  2. T helper cell with specific receptor molecule binds to presented antigen
  3. Once TH cell binds to the presented antigen it is activated. It then rapidly clones by mitosis
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10
Q

Role of TH cell (Helper)

A

1) Specific TH cell binds to the antigen presenting cell
2) Release cytokines that attract phagocytes to the area of infection.
3) Release cytokines that activate Cytotoxic Killer T cell (TC).
4) Activates a specifically complementary B cell.
5) Form memory TH cells
- hundreds of memory TH cells made from one activated TH cell by clonal expansion

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11
Q

Role of Tc cell (Cytotoxic Killer T cell)

A
  • Locate and destroys infected body cells that present the correct antigen.
  • Binds to antigen-presenting-cells
  • Releases perforin (protein) which creates holes in the cell surface membrane which destroys the APC
  • Destroys cancer cells
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12
Q

Humoral Response

A

1) 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).

2) The B cell then differentiates into two types of cell:
-Plasma cells= Produce and secrete vast quantities of specific antibodies into the blood plasma.

Memory (B) cells= Remain in the body to respond to pathogen rapidly and extensively should there be a future re-infection.

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13
Q

Antibodies definition

A

specific protein molecules, that bind specifically to one antigen type

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14
Q

Antibodies shape

A

quaternary structure
four polypeptide chains
“Y-shaped”

  • The main part of the antibody is the same in all antibodies this is the constant region;
  • The variable regions have a different primary structure and therefore a different tertiary structure (different shapes);
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15
Q

What do antibodies and antigens form when they bind?

A

antigen-antibody complex

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16
Q

How do antibodies assist in the destruction of pathogens?

A

1) AGGLUTINATION: Specific antibodies bind to the antigens on pathogen and clump them together.

2) OPSONISATION: marking pathogens so phagocytes recognise and destroy the pathogen more efficiently.

3) LYSIS: Bind to antigens and lead to destruction of the pathogens membrane.

4) ANTI-TOXIN & ANTI-VENOM: Bind to toxins or venom (both usually proteins) to prevent these molecules from binding to their complementary target receptors.

5) Prevent pathogen replication

17
Q

Role of memory cells

A

memory cells are not involved directly in destroying the invading pathogen.

  • 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 more memory B cells.
  • The plasma cells produce lots of the specific antibodies for the invading pathogen, in a short period of time.
18
Q

What is the Secondary response?

A

The activation of memory cells to produce antibodies

The antigen is normally eliminated before it can cause disease or any symptoms develop i.e. the person is “immune” to the disease.
- more antibodies are produced more rapidly

19
Q

What is antigenic variability?

A
  • Some pathogens have antigens which mutate and change shape (e.g. Flu, HIV)
  • pathogen will not be recognised by the memory cells from the previous infection
  • individual will not be able to initiate a secondary response
20
Q

What is passive immunity?

A

No exposure to ANTIGEN. Antibodies are received from elsewhere i.e. are not produced by the individual. Can be given by mother or an antiserum. No production of Memory cells.

21
Q

What is active immunity?

A

Antibodies produced in response to exposure to an ANTIGEN. This type of immunity is provided by the memory cells that are produced after a primary immune response to a pathogen.

22
Q

Describe the difference between active and passive immunity

A
  1. Active involves memory cells, passive does not;
  2. Active involves production of antibody by plasma cells/memory cells;
  3. Passive involves antibody introduced into body from outside/named source;
  4. Active long term, because antibody produced in response to antigen;
  5. Passive short term, because antibody (given) is broken down;
  6. Active (can) take time to develop/work, passive fast acting
23
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 (helper) cell with complementary receptor protein binds to antigen;
  4. T cell stimulates B cell;
  5. (With) complementary antibody on its surface;
  6. B cell secretes large amounts of antibody;
24
Q

Why are vaccines not effective against pathogens?

A

show antigenic variability

25
Q

What is herd immunity?

A

If enough individuals in the population are vaccinated (85%), then there is little chance of the disease spreading, therefore even non-vaccinated individuals will be protected.

26
Q

Ethical issues of vaccines

A
  • animal testing
  • human testing
  • is it available to all
  • balancing risk of side effects against possible benefit
27
Q

Monoclonal Antibodies definition

A

antibodies with same tertiary structures, produced from cloned plasma cells

28
Q

State why some antibodies are referred to as monoclonal

A

produced from cloned plasma cells

29
Q

ELISA Test

A

-Monoclonal antibodies fixed to the surface of the test well.
- Sample containing molecule to be detected or positive control binds to antibody due to complementary shape.
- Second monoclonal antibodies (with enzyme attached) added and also binds to molecule.
- Then washed – so any unbound antibodies with enzyme washed away and removed from test well.
- Substrate added
- Colour change = Positive Result.

30
Q

HIV

A
  1. Protein on HIV binds with a protein commonly found on TH cells.
  2. Capsid fuses with cell-surface membrane and releases Viral mRNA and enzymes into the helper TH cell.
  3. The HIV’s reverse transcriptase converts viral mRNA into cDNA using host nucleotides.
  4. Viral cDNA moves into nucleus of T cell and is inserted into host cell genome (DNA). The person is now INFECTED.
  5. Transcription and translation of this DNA occurs so the T cell starts to manufacture HIV particles.
  6. Particles break away from TH cell with a section of host cell surface membrane which forms their lipid envelope, with TH receptor proteins (to gain access into more TH cells).
  7. Over time this leads to a reduction in the number of TH cells or reduction by inactivation of TH cells.
31
Q

Describe the structure of the human immunodeficiency virus (HIV).

A
  1. RNA
  2. Reverse transcriptase;
  3. (Protein) HIV capsid;
  4. lipid viral envelope
  5. Attachment proteins;
32
Q

Tests using monoclonal antibodies are specific. Use your knowledge of protein structure to explain why.

A
  • Specific primary structure
  • Specific tertiary shape;
  • Only binds to complementary antigen
33
Q

Describe how a person infected with HIV will develop AIDS (if untreated) and die of secondary infections.

A
  • High viral load leads to increased destruction of helper T cells;
  • Less activation of B cells
  • Less production of plasma cells
  • (Less able to) destroy other pathogens
34
Q

Suggest how one antibody can be specific to two different proteins.

A
  1. have a similar tertiary structure;
  2. Antibody is complementary to both
35
Q

Explain how HIV affects the production of antibodies when AIDS develops in a person.

A
  1. Less antibody produced;
  2. (Because HIV) destroys helper T cells;
  3. (So) few B cells activated
36
Q

AIDS

A
  • AIDS is not a pathogen, so cannot be detected using antigens or antibodies.
  • AIDS can be screened for by checking the number of TH cells.
  • HIV does not kill directly but by compromising the immune system it leaves people vulnerable to secondary diseases that ultimately cause death. B memory cells MUST be activated by specific TH cells, which may have been destroyed
37
Q

Consequences of AIDS

A
  • more HIV
  • destruction of more TH cells
  • less activation of B cells
  • less able to destroy pathogen
38
Q

How do antibiotics work?

A
  • Antibiotics work by preventing bacteria making a normal cell wall
  • This means that the bacteria are unable to resist osmotic pressure and the cells burst due
39
Q

Viruses

A
  • Viruses use host cells organelles to carry out metabolic activities so do not have any viral organelles to disrupt.
  • Viruses also have a CAPSID (protein coat) rather than a murein cell wall. This does not allow antibiotics to act on viruses as they do for bacteria.
  • As viruses spend the majority of time within a host cell, they are also out of reach of antibiotics.

Biology (29 decks)

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