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immunology Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is an immune response

A

body invaded by pathogen, series responses ensure pathogen rapidly identified (as non self) & destroyed before damage organism

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2
Q

what is an antigen

A

molecule (usually protein) that stimulates immune response that results in production of a specific antibody e.g. glycoproteins, glycolipids

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3
Q

how does the body know a cell is an own cell rather than foreign/pathogen

A

each cell has specifically shaped antigen on plasma cell surface membrane

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4
Q

what is a phagocyte

A
  • WBC’s that can distinguish between cells that do or do not have correct antigens.
  • engulf & destroy cells with non-self antigens (phagocytosis)
  • detect chemical signals produced by pathogens
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5
Q

what makes phagocytosis non-specific and why is specific immunity needed

A

works same way for any cell/pathogen w non-self antigen. take too long destroy all pathogens in infection, could damage tissues so specific immunity needed

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6
Q

Describe the non-specific defence mechanisms the body may launch against pathogens (5 marks)

A

phagocytosis – No Mark
1. Pathogen is engulfed by the phagocyte.
2. Engulfed pathogen enters the cytoplasm of
the phagocyte in a vesicle;
3. Lysosomes fuse with vesicle releasing
digestive enzymes;
4. Lysosome enzymes break down the pathogen.
5. Waste materials are ejected from the cell by exocytosis;

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7
Q

Describe how a phagocyte destroys a pathogen present in the blood.

A
  1. Engulfs;
  2. Forming vesicle/phagosome and fuses with lysosome;
  3. Enzymes digest/hydrolyse;
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8
Q

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

A
  1. (Cells from) other organisms/transplants;
  2. Abnormal/cancer/tumour (cells);
  3. (Cells) infected by virus;
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9
Q

what do T cells do:

A

responsible for stage of immune response called cellular response.
1) rather than T helper cells responding to pathogen and its antigens directly they bind to antigen presenting cells, with specifically complementary antigen
2) once TH cell ( w specific receptor molecule) bind to antigen it’s activated & rapidly clones by mitosis

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10
Q

the cloned TH daughter cells differentiate into 3 different types of cell:

A

1) TH:
- specific Th cell bind to antigen presenting cell
- release cytokines that attract phagocytes to area infection
- release cytokines that activate cytotoxic killer T cell (Tc)
- activates specifically complementary B cell
- form memory TH cells

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11
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 divides to form clone secreting / producing same antibody;
  7. B cell secretes large amounts of antibody;
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12
Q

Explain how the humoral response leads to immunity

A
  1. B cells specific to the antigen reproduce by mitosis.
  2. B cells produce plasma and memory cells
  3. Second infection produces antibodies in larger quantities AND quicker
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13
Q

describe B cell activation

A
  • TH cell w correct receptor binds presented antigen, locates & activates specifically complementary B cell
  • TH cell release cytokine chemicals that signal B cell clone by mitosis
  • B cell differentiate 2 types cell:
    1. plasma cells - produce & secrete specific antibodies into blood plasma
    2. memory B cells - stay in body, respond pathogen rapidly if another infection
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14
Q

what is the primary response

A

process from initial recognition of pathogen as non-self up to producing antibodies

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15
Q

what is an antibody

A

Protein made in response to foreign antigen – has binding sites which bind specifically to an antigen. specific antibody is produced by specific ‘Plasma cell’.

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16
Q

what is the structure of an antibody?

A
  • quaternary structure made of 4 polypeptide chains
  • Y shape
  • main part same in all (constant region)
  • variable regions(binding sites) have diff primary structure so diff tertiary structure for each antibody
  • specific antibodies only complementary 1 antigen
17
Q

how do antibodies assist in 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

18
Q

Describe and explain the role of antibodies in stimulating phagocytosis.

A
  • Bind to antigen OR Are markers;
  • (Antibodies) cause clumping/agglutination OR Attract phagocytes;
19
Q

what is the secondary response

A

activation of memory cells to produce antibodies
- rapid & extensive
- antigen destroyed before can cause disease (immunity)
- more antibodies produced, more rapidly

20
Q

what is antigenic variability and why is it a problem

A
  • 2ndary response effective, most pathogens same shape antigens, memory cells recognise
  • some pathogens antigens mutate & change shape (e.g flu, HIV)
  • difficult develop vaccine
21
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;
22
Q

what are vaccines

A
  • contain antigens from dead or weakened pathogens
  • stimulate primary response
  • memory cells recognise antigen if re-infection
23
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.

24
Q

vaccine ethical issues

A
  • animal testing
  • human testing…are they being put at risk?
  • accessible to all or only rich?
  • side effects vs possible benefit
  • should be compulsory?
  • loss genetic variability if organism eliminated
25
Q

State why some antibodies are referred to as monoclonal

A

(Antibodies) produced from a single clone of B cells / plasma cells;
OR
(Antibodies) produced from the same B cell / plasma cell;

26
Q

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

A
  • Specific) primary structure / order of amino acids;
  • (Specific) tertiary / 3D structure / shape;
  • (So) Only binds to / fits / complementary to one antigen;
27
Q

uses of monoclonal antibodies

A
  • pregnancy kits, ELISA test
  • killing specific cells
  • targeting drugs
  • diagnosis ( showing presence of specific antigen)
28
Q

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

A
  1. (First) antibody binds/attaches /complementary (in shape) to antigen; 2. (Second) antibody with enzyme attached is added;
  2. (Second) antibody attaches to antigen;
  3. (Substrate/solution added) and colour changes;
29
Q

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

A
  1. RNA (as genetic material);
  2. Reverse transcriptase;
  3. (Protein) capsomeres/capsid;
  4. (Phospho)lipid (viral) envelope OR Envelope made of membrane;
  5. Attachment proteins;
30
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/CD4 cells;
  • Less activation of B cells/cytotoxic T cells/phagocytes;
  • Less production of plasma cells/antibodies OR (With cytotoxic T cells) less able to kill virus infected cells;
  • (More able to) destroy other microbes/pathogens OR (More able to) destroy mutated/cancer cells;
31
Q

how does HIV replicate

A
  1. protein on HIV binds with protein found on TH cells
  2. capsids fuse with cell surface membrane & release viral mRNA & enzymes into TH cell
  3. HIV’s reverse transcriptase convert viral MRNA into cDNA using host nucleotides
  4. viral cDNA move into nucleus of T cell & inserted into host genome. person now infected
  5. transcription & translation of this DNA occur so T cell manufacture HIV particles
  6. particles break away from TH cell w section of host cell surface membrane which forms lipid envelope, w TH receptor proteins
  7. over time reduction in no. TH cells or reduction by inactivation of TH cells
32
Q

how do antibiotics work

A
  • prevent bacteria making normal cell wall
  • unable resist osmotic pressure & cells burst due to increase in cell volume of water by osmosis
  • viruses use host cells organelles to carry out metabolic activities so do not have any viral organelles to disrupt
  • viruses also have capsid rather than murein cell wall , so antibiotics not act on viruses
  • viruses spend most time in host cell, out of reach of antibiotics

biology (7 decks)

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