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A Level Biology Paper 1 > Immunology > Flashcards

Immunology Flashcards

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1
Q

Describe how antibodies are produced in the body following a viral infection

A
  1. virus contains antigen;
  2. virus engulfed by phagocyte / macrophage;
  3. presents antigen to B-cell;
  4. memory cells / B-cell becomes activated;
  5. (divides to) form clones;
  6. by mitosis;
  7. plasma cells produce antibodies;
  8. antibodies specific to antigen;
  9. correct reference to T-cells / cytokines;
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2
Q

What is an antigen

A

Molecule usually a protein
That stimulates an immune response
Resulting in the production of a specific antibody

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3
Q

Pathogen

A

A disease carrying microorganism

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4
Q

How do pathogens cause disease and harm

A

Release toxins which can directly damage tissue

Replicate inside host and destroy it

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5
Q

What do antigens allow the immune system to identify

A 
Pathogens
Toxins
Abnormal body cells
Cells from other organisms of the same species
Foreign cells
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6
Q

Phagocyte

A

Type of leukocyte
Capable of distinguishing between cells that do and don’t display the correct antigens
Detect chemical signals
Engulf and destroy foreign antigen presenting cells through phagocytosis
To become an antigen presenting cell

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7
Q

Phagocytosis

A

Pathogen engulfed by phagocytosis
Enters cytoplasm in a vesicle called a phagosome
Lysosomes fuse with the phagosome
Releasing hydrolysis digestive enzymes called lysozymes
Pathogen hydrolysed
Waste material removes via exocytosis
Phagocyte becomes an antigen presenting cell, displaying the pathogens antigen on its cell surface membranr

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8
Q

What is phagocytosis by definition

A

Part of non specific immunity

Where pathogen is engulfed, hydrolysed and destroyed by a phagocyte

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9
Q

Specific immunity

A

Specific response to a specific antigen on the surface of a cell or pathogen
That has been recognised as non self

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10
Q

What are the stages of cellular response

A

Antigen presenting
Clonal selection
T cells

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11
Q

Explain cellular response

A

Th cells can respond directly to pathogen or respond to an APC that presents the specifically complementary antigen
Phagocytosis means Th cells can bind to the presented antigen
Therefore activated
Then rapidly one by mitosis
In clonal selection

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12
Q

Role of helper T cells

A

Specific Th cell binds to APC and when activated rapidly divide by mitosis for clonal selection
Release cytokines that attract phagocytes to the area of infection
Release cytokines that activate cytotoxic killer T cells
Activate specifically complementary B cell
Form memory Th cells

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13
Q

Cytokines

A

Released by helper T cells
Attract phagocytes to the area of infection
Activate cytotoxic killer T cells

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14
Q

What is the role of cytotoxic killer T cells

A

Locate and destroy infected body cells that present the correct antigens
Bind to APC
Release perforin (protein) which creates holes in the cell surface membrane and causes the APC to be destroyed

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15
Q

Role of memory T cells

A

Remain in the blood long term

Can recognise foreign antigens to respond rapidly and extensively upon second infection

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16
Q

Why is clonal selection needed

A

Wouldn’t be enough room in the body to have lots of every T cell for every antigen you may ever encounter
Increased number of cells woukd increase the total energy demands of organism

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17
Q

Humoral response

A

A stage of primary response
That involves the activation of B cells to produce antibodies
B cells must be stimulated by their complementary Th cell
By the release of cytokines

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18
Q

Explain B cell activation

A

A specific Th cell with the correct receptor binds to presented antigen and locates and activates the specifically complementary B cell
Specific Th cell releases cytokine chemicals which signal the specific B cell to clone by mitosis (clonal selection)
B cell then differentiates into: plasma cells which produce and secrete vast quantities of the specific antibody into the blood
And memory B cells which remain in the body to respond rapidly and extensively if a future reinfection occurs for the same pathogen

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19
Q

Similarities between primary and secondary response

A

Both involve memory B cells

Both involve antibody production

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20
Q

Differences between primary and secondary response

A

P: first time in contact with the pathogen/S: reinfection
P: takes longer to establish immune response/S: rapid and extensive
P: response by naiive B cells and T cells/S: response by memory B cells
P: antibody peak reaches in 7-10 days/S: peak 3-5 days
P: antibody levels decline rapidly/S: remain high for longer time

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21
Q

Types of non specific defenses

A

Physical barriers: mucus, stomach acid, ear wax, blood clotting, lysozyme in tears
Phagocytosis: engulfs and destroys

Immediate response
Same for all pathogens

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22
Q

Types of specific defenses

A

Cell mediated: T lymphocytes
Humoral: B lymphocytes

Slower response
Specific to each pathogen

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23
Q

What is an antibody

A

A quaternary protein made in response to foreign antigens
Has a binding site specific to one antigen
Specific antibody produced by specific plasma cell

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24
Q

Structure of an antibody

A

Quaternary protein of 4 polypeptide chains
Y shape
Constant region that’s the same for all antibodies
Variable region has a different primary structure so different tertiary structure
Variable region where the specific binding site is
Can only form antigen antibody complex with the one
Epitope=specific region of antigen that antibody binds to

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25
4 ways antibodies assist the destruction of a pathogen by preventing its replication
Agglutination Opsonisation Lysis Anti toxins/venom
26
Agglutination
Specific antibodies bind to the antigens on the pathogen and clump them together
27
Opsonisation
Marking pathogens so phagocytes recognise and destroy the pathogen more efficiently
28
Lysis
Bind to antigen and lead to destruction of the pathogens membrane
29
Antitoxin/antivenom
Bind to toxin or venom (protein) | To prevent them binding to their specific complementary target receptors
30
How are B cells activated
Indirectly by specific Th cell with correct receptor that can bind to presented antigen, locate and activate B cell Memory B cells not involved directly in destroying pathogen but on reinfection, rapidly activated by cytokines Directly activated when B cell detects the antigen via antibodies
31
Explain the secondary response
Rapid and extensive Antigen is usually eliminated before it can cause disease or any symptoms to develop More antibodies produced more rapidly Defined as the activation of memory cells to produce antibodies
32
Explain antigenic variation
Random mutations of pathogens antigens Making it hard to develop vaccines since no longer recognisable to memory cells (no longer complementary to receptors) Can't initiate secondary response
33
Passive immunity
Type of immunity where no exposure to antigen Antibodies recieved from elsewhere/not produced by individual No memory cells produced Short term and fast acting
34
Passive immunity examples
Antiserum Placenta Breast feeding and milk
35
Active immunity
Type of immunity where antibodies are produced in response to exposure to an antigen Memory cells produced after a primary immune response Long term but slower acting From contracting an illness and fighting it off or a vaccine
36
Passive vs active immunity
P: No antigen exposure/A: Antigen exposure P: Antibodies not produced by individual and recieved from elsewhere/A: Antibodies produced in response to antigen P: No memory cells produced/A: Memory cells produced after primary immune response P: Short term protection/A: long term P: Antibodies eventually broken down/A: Memory B cells circulate in blood for years P: Fast acting/A: Slower due to primary response
37
How does a vaccine work
Contains antigens from dead, weakened or attenuated pathogen Pathogen engulfed by phagocytes and displayed on the antigen presenting cell Specific T Helper cell binds to APC antigen Stimulates a specific B cell by releasing cytokines B cell divide by mitosis to produce plasma cells and memory cells in clonal selection Plasma cells produce and release the complementary antibody Memory cells recognise antigen on second infection Not effective against pathogens showing antigenic variation
38
Purpose of boosters
Increase effectiveness of vaccinations Acts as a memory cell top up so that on infection there are enough memory cells to divide into plasma cells to combat pathogen with antibodies
39
Outline vaccine ethics
Side effects vs benefits: usually mild causing fever but could be severe and permenant Animal trials and animal rights Human trials: who and how much risk Affordable for everyone Should we be eliminating an organism and loss of generic variation
40
Why don't vaccines provide protection against antigenic variation
Vaccine contain specific antigen of attenuated pathogen So only provide immunity against that pathogen Antigens mutate and can change shape No longer complementary to specific B cell/antibody No secondary immune response
41
What is herd immunity
Enough individuals in a population are vaccinated 85% So little chance of the disease spreading Even non vaccinated individuals protected
42
What are monoclonal antibodies
Antibodies produced from a single group of genetically identical plasma cells With a unique tertiary structure that binds to only one type of antigen
43
Uses of monoclonal antibodies
``` Research Immuno assays (pregnancy or elisa) Diagnosis Targeting drugs Killing specific cells Isolating specific chemicals ```
44
Ethics of monoclonal antibodies
Similar to vaccine ethics Unethical to induce tumours in mice which are genetically engineered to produce human antibodies A few cases of volunteers experiencing unexpected side effects
45
Antigenic drift
Small random mutations of pathogens antigens
46
Antigenic shift
New strain develops from mutation of pathogens antigens
47
True negative
Test says you don't have it | You don't have it
48
True positive
Test says you have it | You have it
49
False negative
Test says you don't have it | You have it
50
False positive
Test says you have it | You don't have it
51
Why do blood transfusions work sometimes but not long term
Blood contains memory cells and plasma cells which can produce and release specific antibodies So transfers antibodies and acts as a form of passive immunity Antibodies can then bind to the specific antigen on pathogen Leading to the destruction of the pathogen in patient Patients immune system will start to break down the plasma cells because seen as foreign So won't provide long term protection because antibodies are destroyed if plasma cells are destroyed
52
What is an ELISA test
Enzyme Linked Immunosorbent Assay A method of measuring the amount of antigen or antibody in a sample Involves monoclonal antibodies with attached enzyme that catalyses an easily detectable substances
53
Explain the process of an ELISA test
Test uses monoclonal antibodies to detect a certain substance in a sample of liquid 1. Monoclonal antibodies fixed to surface of test well 2. sample containing molecule to be detected/positive control binds to antibody due to complementary shapes 3. Second monoclonal antibody with enzyme attached added and binds to molecule (conjugates) 4. Washed to remove any excess unbound antibodies with enzyme to prevent false positive 5. Substrate for enzyme added 6. Chemical colour change visible means that the enzyme is present and hence antibody bound so positive result
54
How does a pregnancy test work
Detects HCG hormone (Human Chorionic Gondatropin) found in the urine of pregnant women 1. Application area contains antibodies for HCG bound to a coloured blue bead 2. Urine applied, any HCG in urine binds to antibody on the beads 3. Forming an antigen-antibody complex 4. Urine moves up the stick to the test strip, carrying any beads with it 5. Test strip contains antibodies to HCG that are immobilised Present: test strip turns blue since immobilised antibody binds to any HCG, concentrating the HCG-antibody complex with the blue bead attached Not present: beads pass through test area without binding to anything so won't go blue
55
Why can antibodies only bind to one type of antigen
Quaternary proteins with a specific 3D tertiary structure determined by the unique primary structure As a result they have 2 unique binding sites complementary in shape to only one type of antigen So only form an antigen-antibody complex with this one type
56
Placebo benefits
Prevents psycology bias | Prevents bias from medical professionals and researchers
57
HIV
Human Immunodeficiency Virus
58
AIDS
Acquired Immune Deficiency Syndrome
59
Structure of HIV
HIV RNA: two identical single stranded RNA molecules containing the genetic material for making more HIV particles Reverse Transcriptase: 2 copies of this enzyme that transcribe the RNA into host DNA once inside the cell Viral envelope: Piece of the plasma membrane budded off the last T helper host cell (phospholipid) Capsid: Bullet shaped protein coat that protects the HIV RNA within Surface glycoproteins: Protein spikes that allow HIV to attach to CD4 receptors on host T helper cell due to complementary shape
60
How does HIV replicate
1. Protein on HIV binds to CD4 receptor protein on T helper cell membrane 2. Capsid fuses with its plasma cell membrane and releases viral mRNA and enzymes into Th cell 3. Reverse transcriptase converts viral mRNA into cDNA using host nucleotides 4. Viral cDNA moves into nucleus of Th cell and is inserted into the host genome 5. Person is now infected 6. Translation of this produces mRNA, then translated so the cell starts to manufacture HIV particles 7. Particles break away from host cell with some of the host cells surface membrane 8. Which forms the viral lipid envelope 9. Over time leads to a reduction in the number of Th cells by inactivation of Th cells
61
How can you tell if someone has HIV or AIDS
Uninfected healthy person should have 800-1200 Th cells per mm cubed of blood If suffering with AIDS, can be as few as 200 Screening for HIV can detect and determine HIV status of patient AIDS isn't a pathogen so can't be detected with antigens or antibodies AIDS screened for by checking the number of Th cells
62
Relationship between HIV and AIDS
HIV causes AIDS
63
What is AIDS
Caused by HIV | Leaving victims vulnerable to secondary diseases and opportunistic infections
64
Symptoms of AIDS
Pneumonia Kaposi's sarcoma (connective tissue cancer) Weight loss Diarrhoea Can develop lung, intestine, brain or eye infections
65
What are antibiotics
Drugs prescribed to treat bacterial infections
66
How do antibiotics work
Prevent bacteria making a normal cell wall of peptidoglycan So bacteria can't resist osmotic pressure Cells burst due to an increase in water volume by osmosis
67
Why don't antibiotics work on viruses
Virus uses host cell organelles to carry out metabolic activities so no viral organelles to disrupt Since usually in host cell they are out of reach of antibiotics Have a capsid not murein cell wall which does not allow antibiotics to act on viruses as they do bacteria
68
How can HIV lead to death
Doesn't directly kill but compromises the immune system and leaves people vulnerable to secondary diseases and opportunistic infections that ultimately cause death B memory cells must be activated by Th cells, which may have been destroyed therefore can't carry out a secondary immune response
69
What are T cells and why are they called that
T lymphocytes Responsible for the stage in the immune system called the cellular response Primarily produced in the thymus
70
What are B cells and why are they called that
B lymphocytes Type of leukocyte responsible for producing and releasing antibodies in the humoral response Produced in the bone marrow
71
Active natural immunity
Immune after catching a disease
72
Active artificial immunity
Immune after vaccine
73
Passive natural immunity
Body immune from antibodies from placenta/breast milk
74
Passive artificial immunity
Immune after injected with antibodies from someone else/monoclonal antibodies
75
Full function of memory cells
Remain in circulation in case of future reinfection of the same pathogen If they encounter the antigen again they are rapidly activated by cytokines secreted by specific Th cells and rapidly divide by mitosis Producing lots of antibodies in a short time frame
76
Latent
Virus is there but doesn't replicate
77
Viron
Infectious virus particle that can enter host cell and replicate
78
Retrovirus
Single stranded RNA inside virus

A Level Biology Paper 1 (16 decks)

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