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Biology 3/4 > Unit 4 AOS3 > Flashcards

Unit 4 AOS3 Flashcards

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1
Q

Pathogen

A

An agent that causes disease.

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2
Q

Antigen

A

Any molecule that triggers an immune response.
(Interacts with immune system).

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3
Q

Allergen

A

Non-pathogenic antigen that triggers an allergic reaction.

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4
Q

How does the immune system protect the body?

A

By scanning and destroying pathogens.

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5
Q

2 antigen types

A
  • Self-antigens.
  • Non-self antigens.
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6
Q

Self-antigens

A

Located on the surface of cells, mark the cell as ‘self’ so the immune system doesn’t attack.
MHC I markers
MHC II markers.

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7
Q

MHC I markers

A

Expressed on all nucleated cells; Identifies cells as self.

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8
Q

MHC II markers

A

Found on specialised cells of the immune system,

Allow antigen-presenting cells to show T helper cells foreign antigens which in turn kicks of the adaptive immune response.

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9
Q

MHC

A

Major Histocompatibility Complex Proteins

MHC proteins differ between individuals.

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10
Q

Non-self antigen

A

A molecule from outside the body that is recognised by the immune system and initiates an immune response attack.

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11
Q

Malfunctions involving antigens

A

The immune system results in the recognition of self-antigens as non-self. So immune system attacks self-cells; healthy cells (Autoimmune disease)

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12
Q

Red Blood Cells

A

Red blood cells have no MHC proteins.
Type A —> A antibodies.

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13
Q

Types of Pathogens

A

Cellular and Non-cellular pathogens.

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14
Q

Cellular pathogens

A

cellular structure + living organism
- Bacteria.
- Fungi.
- Worms.
- Protozoa.

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15
Q

Bacteria

A
  • Unicellular prokaryotes.
  • Cause disease through toxins and enzymes. Affecting the functioning of cells or causing death.
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16
Q

Fungi

A
  • Eukaryotic
  • Yeast, moulds containing filaments called hyphae
    Thrush and Ringworm
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17
Q

Worms

A
  • Multicellular invertebrate.
  • Egg, larval + adult stages.
  • 55m
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18
Q

Protozoa

A
  • Single-cell eukaryotic.
  • Free-living or parasitic.
  • Inhibit nucleic acid synthesis, protein synthesis and cellular respiration.
    eg. Malaria.
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19
Q

Non-cellular pathogens

A
  • Viruses
  • Prions.
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20
Q

Viruses

A
  • Composed of genetic material inside a protein coat, sometimes covered in a lipid envelope.
  • Not able to independently reproduce, so they insert genetic material into the host’s cell used for cell replication.
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21
Q

Prions

A
  • Abnormally folded proteins with the ability to induce normal proteins to become misfolded.
  • Only occurs in mammals and affects the brain and other neural structures.
  • Contain no nucleic acids.
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22
Q

First Line of Defence

A

Physical, chemical and microbiological barriers preventing pathogenic invasion.

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23
Q

Innate immune system

A

Component of an immune system composed of generalised and non-specific defences and/or response to pathogens.
1st and 2nd line of defence.

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24
Q

Barriers in plants

A
  • Physical.
  • Chemical.
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25
Q

Physical Barriers in Plants

A

Prevent pathogens from physically entering.
- Thick bark.
- Thorns.
- Closing of the stomata.
- Waxy cuticles on leaves.
- Galls formation.

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26
Q

Chemical Barries in Plants

A

Production of chemicals harmful to pathogens.
- Chitinases; antifungal
- Phenols

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27
Q

Barriers in animals

A
  • Physical.
  • Chemical.
  • Microbiological.
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28
Q

Physical Barriers in Animals

A

Block pathogens.
- Intact Skin.
- Mucous secretions // Hairs on the respiratory tract

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29
Q

Chemical Barriers in Animals

A

Chemicals make an unliveable environment.
- Low pH in Vagina.
- Lysozyme in tears.
- Acidic sweat.
- Stomach acid.

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30
Q

Microbiological Barriers in Animals

A

Non-pathogenic bacteria prevent the growth of pathogentic bacteria. “Normal flora” –> bacteria on skin etc.

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31
Q

Second line of Defence

A

Needed when pathogens slip by the first line.

Characterised by the non-specific and immediate response to injury and pathogens by cells and molecules –> destroy pathogens.

2 components : Cellular + Non-cellular.

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32
Q

Cellular components (2nd line)

A

All cells involved are leukocytes (white blood cells that protect the body from pathogens).
- Phagocytes.
- Natural Killer Cells.
- Mast Cells.
- Eosinophils.

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33
Q

Phagocytes

A

Cells that engage in phagocytosis which they consume and destroy foreign/dead material, engulfing it by endocytosis. Lysosomes then destroy the material.
- Neutrophil.
- Macrophage.
- Dendritic cell.

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34
Q

Neutrophil

A

Engages in phagocytosis of pathogens and foreign material, as well as the release of cytokines.

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35
Q

Macrophage

A

Leukocyte that engages in phagocytosis and antigen presentation. (present antigens on outside of cell from consumed)

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36
Q

Dendritic cell

A

Type of leukocyte that engages in phagocytosis and antigen presentation. (present antigens on outside of cell from consumed)

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37
Q

antigen-presenting cell

A

A subgroup of phagocytes that display antigens (MHC II) from consumed pathogens on their surface and interact with the adaptive immune system.

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38
Q

Process of phagocytosis + antigen presentation

A
  1. Phagocytosis of pathogen.
  2. Fusion with lysosome.
  3. Enzymes start to degrade pathogen.
  4. Pathogen breaks down into smaller fragments.
  5. Fragments of antigen are presented on cell surface.
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39
Q

Why are cytokines produced?

A

Phagocytes release them to communicate in the immune system.

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40
Q

What are cytokines?

A

Cell signalling molecules that aid in communication between immune cells and help protect against pathogens.

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41
Q

Natural Killer Cells

A

Responsible for the recognition and destruction of damaged and/or infected host cells (abnormally + virally infected).

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42
Q

2 Natural killer cell receptors

A

Killer inhibitory receptor; Exaimes cells surface for MHC I markers.
Killer activation receptor; Binds to certain molecules that appear on cells undergoing cellular stress.

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43
Q

Mast cells

A

Type of leukocyte responsible for relasing histamines (play a key role in inflammation) during allergic + inflammation responses (in result to infections)

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44
Q

Eosinophils

A

Large granulated cells contain various toxic chemical mediators that help destroy invading pathogens.
- Target pathogens too large to be phagocytosed.

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45
Q

Noncellular components (2nd Line)

A

Other key molecules/processes.
- Interferons.
- Complement proteins.
- Fever.

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46
Q

Interferons

A

Cytosine released by virally infected cells increases the viral resistance of neighbouring unaffected cells.
- Interact with receptors on neighbouring cells to make them less susceptible to viral infection. (prevent spread).

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47
Q

Complement proteins

A

Different proteins found in the blood that opsonise, cause lysis and attract phagocytes to invading pathogens. Complement cascade occurs.

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48
Q

Complement Cascade

A

Complex sequence of events where proteins react with each other after the activation of complement proteins.

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49
Q

3 major outcomes of the complement cascade

A
  • Opsonisation
  • Chemotaxis
  • Lysis
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50
Q

Opsonisation

A

Complement proteins attach to the surface of pathogens making them easier to phagocytose (to recognise as foreign)

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51
Q

Chemotaxis

A

Complement proteins gather near pathogens and attract phagocytes.

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52
Q

Lysis

A

Complement proteins join on the surface forming a membrane attack complex (MAC) to create pores. This destroys pathogens by causing lysis via influent or fluid into pathogenic causing it to burst.

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53
Q

Fever

A

Temporary increase in body temperature.
Shivering + heat-conserving behaviours.

54
Q

Steps in inflammatory response

A
  1. Initiation.
  2. Vasodilation.
  3. Migration.
55
Q

Initiation

A

Response to an injury; immune cells in tissue and damaged cells release cytokines.
Mast cells degranulate and release histamines.

56
Q

Vasodilation

A

Histamine travels to nearby blood vessels binding to specific receptors causing vasodilation to increase blood flow. (redness + swelling).
- Formation of gaps increases permeability to cells of the immune system.

57
Q

Migration

A

Vasodilation allows for innate immune system components to leave the bloodstream and enter the injury site.
Components:
- Phagocytes; phagocytose pathogens
- Complement proteins; attract pathogens and help phagocytes destroy them.

58
Q

Pus

A

Contains dead immune cells and pathogens.

59
Q

The third line of defence

A

“Adaptive immune system”
- Humoral and cell-mediated responses that create specific immune responses and immunological memory.

60
Q

Initiation of 3rd line of defence

A

Combat and destroy pathogens that have breached 1st line.
2 unique features:
- Specificity - responds to each distinct pathogen.
- Immunological memory - allows the body to respond to future re-infections.

61
Q

Immunological memory

A

The immune system quickly combats previously encountered pathogens due to the presence of T and B cells.

62
Q

Antigen Presentation

A

Key process in initiating adaptive immune response involving T lymphocyte called T helper cell via antigen presentation.

63
Q

T lymphocyte

A

Plays an important role in cell-mediated immunity. Differentiates into cytotoxic T cells, T memory cells and T helper cells.

64
Q

T helper cells

A

A differentiated T lymphocyte supporting the functioning of a number of different immune cells; the cloning and differentiation of selected T and B cells.

65
Q

What does antigen presentation do in 3rd Line?

A

AP cells engulf and digest pathogens, displaying antigens on MHC II markers.
Then: Travel to the lymphatic system to lymph nodes presenting foreign antigens that interact with complimentary T cell receptors on T helper cells.
—> T helper cells become selected and help initiate adaptive immune response via humoral or cell-mediated immune response.

66
Q

Lymphatic system

A

Vessels and tissue networks form an important component of circulatory + immune system.

67
Q

Lymph node

A

Small secondary tissue of the lymphatic system where antigen-presenting cells activate the adaptive immune system.

68
Q

Humoral Immunity

A

A response where extracellular pathogens are targeted by specific antibodies produced by plasma cells. (B-cell immunity).

Neutralisation + destruction of extracellular pathogens via production and secretion of antibodies.

69
Q

Cell-mediated immunity

A

A response where infected/abnormal cells are destroyed by cytotoxic T cells. (T cell immunity)

70
Q

B-lymphocytes

A

Key mediators:
- Surface covered in B-cell receptors on antibodies.
- In Bloodstream.
- Activation occurs via interaction with pathogenic antigens and T helper cells.

71
Q

Humoral response steps

A
  1. (Selection) Pathogen w/ complementary antigen to B cells interact and B cell is selected.
  2. (Expansion) T helper cells recognise selected B cells and secrete cytokines causing them to undergo clonal expansion.
  3. (Differentiation) T helper cells stimulate selected B cells via cytokines undergoing differentiation. Clones of B cells become B memory cells or plasma cells.
  4. Plasma cells –> secrete antibodies into the blood to defend themselves.
    B memory cells –> reside in the body (prolonged period of time) and are responsible for immunological memory.
72
Q

Antibodies released by plasma cells…

A

Are proteins; 4 polypeptide chains –> 2 heavy and 2 light.
Constant region + Variable regions; when regions bind together and form 2 identical antigen binding sites to allow them to bind to antigens on pathogens.

73
Q

Key functions of antibodies

A
  • Neutralisation.
  • Agglutination.
  • Immobilisation.
  • Opsonisation.
  • Activation of complement proteins.
74
Q

Neutralisation.

A

Antibodies block sites of pathogens used to attack host cells

Can block toxins’ active sites.

75
Q

Agglutination.

A

Antibodies bind with antigens or 2 separate pathogens forming anti-body complexes to make it easier for phagocytosis

76
Q

Immobilisation.

A

Restrict movement of pathogens from formation of large antigen-antibody complexes.

77
Q

Opsonisation.

A

Bind directly to the surface of the pathogen to make it easier to phagocytose.

78
Q

Activation of complement proteins.

A

Antibodies attached to the surface of pathogens facilitate the actions of complement proteins. Including MAC

79
Q

Clonal selection

A

Selecting specific T helper cells and B cells.

80
Q

Cell-mediated immunity

A

Deconstruction of infected or abnormal cells via clonal selection of a cytotoxic T cell.

81
Q

Cytotoxic T cell

A

Differentiated T lymphocytes are responsible for the destruction of infected/abnormal cells.

In Infected cells, MHC I markers MAY present foreign viral antigens on the surface detected by cytotoxic T cells.

82
Q

Cell-mediated Immune response steps

A
  1. Antigen-presenting cells encounter the pathogen and take up the antigen initiating clonal selection.
  2. Clones of selected T cells differentiate into either:
    T memory cells; help form immunological memory.
    Cytotoxic T cells; leave lymph nodes and reach inflammation site.
  3. Cyto T cells at infection site with specific T cells to foreign antigens and bind to abnormal cells.
83
Q

Immunological memory B and T cells

A

B and T cells from adaptive immune response stay in the immune system to respond to previously encountered pathogens.

84
Q

B memory cells

A

Form new antibody-producing plasma cells when antigen matches receptor.

85
Q

T memory cells

A

Into T helper cells and cytotoxic T cells stimulated by antigen-presenting cells on previously encountered antigens.

86
Q

Advantages of Immunological Memory

A
  • Rapid + effective immune response upon re-infection.
  • Prevent formation of disease; pathogen can no longer replicate fast enough to cause disease.
87
Q

What is the lymphatic system?

A

A large network of vessels throughout the body forms circulatory and immune systems.
2 Primary functions:
- Transport antigen-presenting cells and pathogens.
- Location of clonal selection.

88
Q

Functions of the lymphatic system

A
  • Transport antigen-presenting cells to secondary lymphoid tissues “for recognition and initiation of adaptive immune response.”
  • Produce Leukocytes.
  • Removal of fluid from tissues.
  • Absorb fatty acids.
89
Q

Primary Lymphoid tissue

A

Production and maturation of lymphocytes (B + T) in bone marrow.
- Thymus.
- Bone marrow in Long Bones.

B lymphocytes remain in the bone marrow to mature further.
T lymphocytes travel to the thymus to mature.

90
Q

Why do lymphocytes mature?

A

To determine what type it will be.

91
Q

Secondary lymphoid tissue

A

Responsible for maintaining mature lymphocytes initiating adaptive immune response.
Main tissues:
- Lymph nodes
- Spleen.

92
Q

What occurs in secondary lymphoid tissues?

A

Mature lymphoids are clustered and ‘scan’ passing lymph for pathogens or antigen-presenting cells.

Foreign antigen matches receptors on specific lymphocytes causing clonal selection + differentiation where T and B cells are created resulting in swelling of lymphoids.

93
Q

Stages of the lymphatic system

A
  1. Lymphatic drainage.
  2. Lymphatic flow.
  3. Lymphatic surveillance.
94
Q

Lymphatic drainage

A

Blood vessels leak into tissue, and lymphatic capillaries(small vessels) collect fluid(lymph) in tissues and pathogens and transports it to lymph nodes.

95
Q

Lymphatic flow

A

The small lymphatic capillaries join to form larger vessels containing increasing lymph.

It has thin walls and relies on muscle movement to squeeze lymph through the system.
(heart not responsible for pumping).
AWAY FROM LYMPH NODES.

96
Q

Lymphatic surveillance

A
  • Fluid from tissues arrives at lymph nodes via afferent lymphatic vessels. Travelling through B and T cell clusters.
  • Pathogen+antigen presenting meet lymphocyte and bind initiating clonal selection.
  • Adpative immune system activated = exit lymph nodes via efferent lymphatic vessels.
  • Lymph then returned to circulation delaying the launch adaptive immune system *(slower to activate).
97
Q

Natural Immunity

A

Protection against disease formed without medical intervention.
2 Types:
Natural Passive
Natural Active

98
Q

Active Immunity

A

Own adaptive immune system develops antibodies and memory cells to a particular antigen.

99
Q

Passive Immunity

A

Immunity is created by antibodies from an external source.

100
Q

Natural active immunity

A

Own immune system encounters pathogen creating antibodies and memory cells specific to that pathogen.
Next time encounter the same pathogen it will be destroyed rapidly.

101
Q

Natural passive Immunity

A

Antibodies from natural external sources.
2 methods:
Breastfeeding: Ingested antibodies absorbed into the baby’s bloodstream. (poor adaptive immune response).
Placenta: Antibodies cross through and enter the foetus’s bloodstream via the umbilical cord.

102
Q

Artificial Immunity

A

Immunity developed from medical intervention creating antibodies and memory cells.
- Artificial active
- Artificial passive.

103
Q

Artificial active immunity

A

Own adaptive immune system produces antibodies and memory cells due to medical intervention.
–> Vaccinations.

104
Q

Vaccines

A

prompt an adaptive immune response to make memory cells.

105
Q

Primary immune response

A

First Vaccine; delays adaptive immune system response –> antigen-presenting cells find complementary B and T cells to vaccine antigens (these B&T diminish over time).

Reaction to antigen not previously exposed to.

106
Q

Secondary immune response

A

Second vaccine; memory cells recognise antigens in the vaccine and mount rapidly generating long-lasting immunity (antibodies + memory cells).

107
Q

Booster Vaccines

A

Generate more antibodies and memory cells

108
Q

Artificial passive immunity

A

Acquire antibodies from an external source through medical intervention.
Antibodies or antivenom are injected but don’t last long due to no memory cells.

109
Q

Herd Immunity

A

Majority of people within a community are immune to a particular pathogen preventing the spread (can’t be easily reproduced).

110
Q

Infectious disease

A

Caused by pathogens that harm their host and can be transmitted to others.

111
Q

How do infectious diseases impact the population

A

How Contagious the pathogen is; how easily it is transmitted.
How Virulent then pathogen is; how severe disease/harm is from the pathogen.

112
Q

Emerging diseases

A

Haven’t occurred before in humans.
- COVID 19
- Influenza.

113
Q

Re-emerging diseases

A

Once major public health problems declined but are again becoming health problems.
- Ebola.
- Measles.

114
Q

Where do diseases(emerging and re-emerging) come from?

A
  • Evolution of causative organism.
  • Globalisation and travel.
  • Exposure of humans to animals (zoonosis).
  • Increased human population.
  • Changing technology.
  • Insufficient population vaccines.
115
Q

Epidemic

A

Dramatically increase the occurrence of disease in a specific population in a specific location at a particular time.

116
Q

Pandemic

A

An Epidemic that has spread across multiple countries and/or continents. Affecting a large number of people.

117
Q

Pathogens were introduced by European arrival to Australia.

A
  • Lack of immunity in Indigenous Populations.
  • Lack of knowledge and experience of new pathogens.
  • Disruption caused by colonisation; access to food and water was denied; forced into camps increasing infection,
118
Q

Methods of Identifying Pathogens

A

Physical; Visulise pathogen structure via microscope.
Phenotype; Selective media –> agar plate allows certain pathogens to grow.
Immunological; Serology –> diagnosis based on the presence of antigens or antibodies.
Molecular; Hybirdisation-based detection.

119
Q

Methods of disease transmission

A
  • Airborne transmission.
  • Droplet transmission.
  • Direct physical contact transmission.
  • Indirect physical contact transmission.
  • Faecal-oral transmission.
120
Q

Controlling disease transmission

A

Identification, prevention, control the spread and treatment.

121
Q

Key strategies to control disease transmission

A
  • Prevention; Hygiene sanitation
  • Screening; routine testing
  • Quarantine + Isolation
  • Identification Pathogen
  • Control transmission
  • Treating Infected; Antibiotics
122
Q

Immunotherapy

A

Medical interventions that treat disease by modulating the immune system by amplifying or reducing the immune response

Activation immunotherapies: Induce/Amplify immune response. (also helps recognise cancer cells and destroy them)
Suppression immunotherapies: prevent/reduce an immune response.

123
Q

Monoclonal antibodies

A
  • Lab-made bind to specific antigens.
  • Target specific types of parts of the cell.
  • Used to treat cancer and autoimmune diseases.
124
Q

How are monoclonal antibodies produced?

A
  1. Identify and isolate the target antigen.
  2. Vaccinate an animal with that antigen.
  3. Harvest resulting B cells(produce antibodies).
  4. Fuse B cells into myeloma cells to create hybridoma cells capable of growing and making desired antibodies.
  5. Screen tissue culture for cells that meet requirements and clone them.
  6. Collect and purify antibodies.
125
Q

Cancer

A

Complex group of diseases caused by uncontrolled and unregulated replication of cells that evade other sites.

126
Q

2 types of monoclonal antibodies in immunotherapy

A

Naked monoclonal antibodies; mono antibodies with no other molecules attached to it.
Conjugated monoclonal antibodies; Mono antibodies with molecules attached.

127
Q

Monoclonal antibodies vs cancer

A

naked + conjugated

Attach to cancer cells, stimulating natural killer cells to stimulate and interact with complement proteins or recruitment of leukocytes.
Reduce their ability to hide by blocking immune checkpoint molecules, blocking cell growth.

128
Q

Autoimmune disease

A

Normally: Lymphocytes recognise markers.

In autoimmune diseases, lymphocytes fail to recognise self-makers.

129
Q

Suppression Immunotherapy

A

Dampen immune system and reduce it’s ability to attack self-cells.
Monoclonal antibodies reduce the immune system through:
Cytokine Inhibitation –> binds to and inhibits cytokines.
B cell and T cell depletion and inhibition

130
Q

Immunotherapy and traditional autoimmune disease treatment

A

major autoimmune diseases have no cure.
- Doctors reduce symptoms.
- Suppress the whole immune system.
Traditional autoimmune treatment can become insufficient and develop infections and cancer.

Biology 3/4 (6 decks)

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