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Bio 3/4 > unit 4 aos 1 > Flashcards

unit 4 aos 1 Flashcards

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1
Q

self vs non self cells

A

self: cells & molecules that make up your own body, contain MHC 1 markers to identify cells as self
non-self: refers to everything else, eg. antigens

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2
Q

antigen

A

unique molecule found on the surface of pathogens that initiates an immune response
they are used to recognise if a cell/molecule is self or non-self, if non-self, an immune response is initiated
> allergen: antigens that trigger allergic response.

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3
Q

self antigens (markers)

A

found on the surface of cells and mark them as ‘self’ so that the immune system doesn’t attack them

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4
Q

non self antigens

A

recognised by the leukocyte (wbc), immune system tries to eliminate if detected in the body

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5
Q

pathogen

A

microorganism capable of causing disease or harm. secrete toxins, wich create an immune response

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6
Q

what happens when a pathogen enters- innate immunity

A
  • blood is directed to the site (inflammation)
  • fever
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7
Q

types of cellular pathogens

A

have a cellular structure & are living organisms
- bacteria: unicellular, cause disease through neurotoxins & endotoxins
- fungi: eukaryotic, yeast & moulds
- parasites: live off a host organism while causing the host harm
- protists: eukaryotic, inhibit nucleic acid synthesis & stages of cellular respiration

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8
Q

types of non-cellular pathogens

A

non-living, do not have a cellular structure
- viruses: insert genetic material into a host cell and use the cell to replicate, eg. influenza
- prions: abnormally folded proteins that can infect other proteins, causing them to misfold

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9
Q

physical barriers to infection in animals

A

barriers that block or hinder pathogens from entering an organism
- intact skin
- mucous membranes/secretions
- hair/oils/wax
- expulsion reflexes

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10
Q

physical barriers to infection in plants

A

prevent pathogens from entering the organism
- thick bark
- waxy cuticle
- close stomata

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11
Q

chemical barriers to infection in animals

A

barriers that produce chemical substances that make an environment unliveable for a pathogen.
- lysosome enzymes in tears and saliva
- hydrochloric (stomach) acid destroys pathogens that have been eaten/ swallowed
- acidic sweat that destroys pathogens growing on the surface of the body
- antibacterial compounds in earwax

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12
Q

chemical barriers to infection in plants

A

involve the production of chemicals/ enzymes which are harmful to the pathogen & affect its functioning
- chitnases (antifungal properties)
- phenols (secreted by wounded plants, repelling invading microorganisms)
- trichomes

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13
Q

microbiota barriers to infection

A

presence of non-pathogenic bacteria in the body/plant that prevents the growth of pathogenic bacteria as they compete for space & nutrients
- on the skin, lower gastrointestinal tract and the vagina

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14
Q

the second line of defence (innate immune response)

A

innate immune response which destroys any pathogens which have entered the body
- non-specific, rapid, no immunological memory
- responds in the same way regardless of the type of pathogen or antigen present.

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15
Q

what triggers the inflammatory response

A

mast cells release histamine to initiate inflammatory response.
release of histamine causes:
- vasodilation (dilation of blood vessels)
- increased permeability of blood vessels
- chemoattractant to phagocytes (attract phagocytes to the area)

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16
Q

steps of the inflammatory response

A
  1. initiation- pathogen gets in the body,breaching first LOD, damaged cells release cytokines, attracting neutrophils, which trigger mast cells to release histamine
  2. vasodilation- mast cells degranulate releasing histamine- causes vasodilation, increased permeability of blood, meaning inc. bloodflow and more phagocytes can enter. swelling, redness and warmth in the area
  3. migration- more immune cells travel to infection site, wound is blocked by platelets & clotting factors
  4. repair- cytokines signal neutrophils to phagocytose the pathogens, new cells form underneath wound
    > continues until infection/pathogen is cleared
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17
Q

symptoms of the inflammatory response

A
  • increased blood flow (vasodilation)
  • increased permeability of blood
  • redness
  • swelling
  • heat
  • pain
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18
Q

mast cells

A

cause the inflammatory response
- leukocytes embedded in connective tissue, they become activated when they detect injury to surrounding cells, degranulate to release histamine, which causes:
- vasodilation of blood vessels (more blood flow)
- increased permeability of blood vessels (leukocytes can get out)
- chemoattractant to phagocytes

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19
Q

MHC 1 & MHC 2

A

major histocompatibility complex- bind to antigens and present them to T cells
- MHC 1 markers: self markers found on all nucleated cells
- MHC 2 markers: self markers only found on APCs (macrophages, dendritic cells, B lymphocytes), activate helper T cells of the adaptive immune response

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20
Q

phagocyte & types

A
  • consume and destroy foreign or dead material
  • engulf & break down pathogens
  • engage in phagocytosis
  • Release cytokines that attract additional immune cells to the site of infection
    > neutrophils: granulocyte, disrupts pathogen cell membrane, die after phagocytosis (pus)
    > macrophages: big eater, phagocytose a large number of pathogens that have been agglutinated. APC presenting antigens on MHCII markers, flagging the 3 LOD
    > dendritic cells: APC, better than macrophages, presenting antigens on MHCII markers, flagging the 3 LOD, has grooves/shoots on the outside increase SA
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21
Q

natural killer cells (NK)

A
  • granulocytes, type of lymphocyte
  • destroy cells presenting a non-self antigen on their MHC 1 markers by causing them to undergo involuntary apoptosis
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22
Q

cytokines

A
  • signalling molecules
  • released in response to cell damage or presence of a pathogen
  • promote antibody response & activate macrophages
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23
Q

eosinophils

A
  • granulocytes which can stimulate degranulation of mast cells
  • contain chemicals which help destroy large invading pathogens
  • target pathogens too big to be phagocytosed such as multicellular parasites
24
Q

interferons

A
  • type of cytokine
  • signalling molecules released from virus-infected host cells
  • attract NK cells and produce enzymes that break down viral RNA
  • interact with MHC1 receptors on nearby cells, causing them to heighten their antivirus defences, making them less susceptible to viral infection
  • non-specific, act on any virus
25
Q

complement proteins

A
  • float around the blood inactively, once they become activated as part of innate immune response, they:
  • act as chemoattractants (attract phagocytes)
  • opsonise bacteria (mark it for destruction)
  • form a cell destroying membrane attack complex (MAC) which kills bacteria
  • agglutinate (clump together antigen bearing agents)
26
Q

the third line of defence

A
  • adaptive immune system
  • specific: unique response to each pathogen
  • two immune responses: humoral response (B lymphocytes), and cell mediated response (cytotoxic T cells)
  • immunological memory: immune system remembers the pathogen and produces cells that allow the body to respond better to future reinfections
27
Q

T Lymphocytes & B Lymphocytes

A

T lymphocyte differentiates into:
- cytotoxic T cell
- T helper cell
- memory cell
B lymphocyte differentiates into
- B memory cell
- plasma cell

28
Q

antigen presentation initiating 3rd LOD

A
  • initiates the 3rd LOD
  • APC (macrophage or dendritic cell) engulfs a pathogen and will present one of its antigens on its MHC 2 marker
  • APC then travels through lymphatic system to lymph nodes to present the foreign antigen to helper T cells
  • T helper interacts with MHC 2 marker, initiating specific immune response
29
Q

cell mediated immune response

A
  • destruction of infected cells by cytotoxic T cells
  • antigen is presented on MHCII markers to a T helper cell with matching T cell receptors in the lymph nodes
  • the Th will secrete a cytokine which stimulates the Th to undergo clonal expansion
  • the antigen is also presented to cytotoxic T cells with matching receptors, and the cytokines released by Th will cause CTC to undergo clonal expansion
  • the cloned cytotoxic T cells will then travel around the body and cause apoptosis in infected cells presenting the same antigens on their MHC1 markers.
30
Q

humoral immune response

A
  • involves B lymphocytes with antibodies attached in the lymph
    if B lymphocyte presents antigen:
  • B cell engulfs pathogen with matching antibodies and presents its antigens on MHCII markers in the lymph node
  • Th cell with complementary t cell receptors binds to the antigen, activating the Th, causing it to release cytokines which cause the B cell to undergo clonal expansion into Bm or plasma cell.
  • plasma cells release antibodies, which travel through the blood and agglutinate pathogens with matching antigens
    If another APC presents antigen:
  • APC presents antigen on its MHC II markers in the lymph node
  • Th with complementary T cell receptors binds, releasing cytokines which attract B cells to bind to the APC
  • the cytokines released by the Th cause the B cell to undergo clonal expansion –> Bm or plasma cell
  • specific antibodies created
31
Q

memory b cell

A
  • derived from activated b lymphocytes
  • long living, provide lasting immunity against a specific pathogens antigens so that it can quickly be destroyed if it invades again
  • immunological memory
32
Q

plasma (B) cell

A
  • derived from activated b lymphocytes
  • short living
  • produce 10,000 antibodies per second
    > destroy pathogens via agglutination, sticking them together and flagging for destruction (opsonize)
33
Q

structure of an antibody

A
  • 2 heavy chains (inside Y chain, longer)
  • 2 light chains (outside, shorter)
  • constant region at bottom and variable region at top
    > variable region is diff for each pathogen –> specific
  • antigen binding site
34
Q

primary immune response

A

the first exposure to the pathogen, when the humoral or cell mediated immune response occurs

35
Q

secondary immune response

A

memory b cells enable a fast and efficient immune response if the pathogen invades again, destroying it quickly without having to undergo humoral or cell mediated response again
> faster & more immediate that primary due to Bm
> more antibodies produced

36
Q

strategies for acquiring immunity

A
  • active immunity: protection provided by individuals own immune response > long lasting
  • passive immunity: protection provided by the transfer of antibodies produced by another organism > temporary
37
Q

types of active immunity

A
  • natural: antibodies created by your own immune system in response to a pathogen > creates memory cells > long lasting immunity. eg. covid, influenza
  • artificial: own immune system produces antibodies & memory cells in response to medical intervention. eg. vaccine
38
Q

types of passive immunity

A
  • natural: acquired when you receive antibodies from an external, natural, non-medical source > temporary immunity. eg. mothers breast milk & placenta
  • artificial: acquired antibodies from an external source via medical intervention > temporary. eg. antivenin
39
Q

lymphatic system

A

network of blind ended vessels that collect tissue fluid and drain it back to the circulatory system.
- transports immune cells, where antigen recognition by lymphocytes occurs
- Transports lymphocytes and antigen presenting cells to the lymph nodes in lymph, stimulating the Adaptive Immune Response
- lymph flows through lymph vessels as a result of movement of body muscles

40
Q

primary lymphoid tissues

A

those in which lymphocytes are formed & mature
- bone marrow
- thymus
> all lymphocytes formed in the bone marrow
> t lymphocytes then leave and mature in the thymus

41
Q

vaccinations

A
  • expose someone to an antigen, so that they have an immune response and acquire artificial immunity to that pathogen if it invades the body
  • aim to decrease rates of infection & eradicate disease
42
Q

immunotherapy

A

any treatment that activates or suppresses the immune system to fight disease

43
Q

secondary lymphoid tissue

A

lymph nodes
- where lymphocytes reside
> where lymphocytes are highly concentrated
> filters the lymph flowing back towards the heart
> makes it easier for antigens to encounter B and T lymphocytes, as bacteria flowing through the lymph nodes can be picked up by B and T cells and destroyed by immune response

44
Q

types of vaccinations

A
  • whole pathogen vaccines
  • inactivated vaccines: whole bacteria or viruses that have been altered so that they cant reproduce
  • live attenuated vaccines: bacteria or viruses that have been weakened so it is not as virulent, cause a stronger immune response
  • subunit vaccines: fragments of pathogens that are genetically modified, provide long term immunity
    > recombinant protein vaccines- modify harmless bacteria
    > toxoid vaccines- inactive toxin
    > virus like particles
    > outer membrane vesicles
45
Q

herd immunity

A

when a large proportion of the population has immunity to a disease, there is a lower chance that the pathogen will spread, even people who are not vaccinated will be less likely to contract the disease. protects those who cannot provide their own immunity (immunocompromised, babies)
> virus spreads less effectively, reduced number of susceptible hosts
> booster vaccines result in a secondary immune response to produce more memory cells

46
Q

how do emerging diseases occur

A
  • zoonosis: disease moves from one species to another. pathogen that has mutated with an animal. eg. swine flu
  • antigenic drift: small changes the surface proteins that antibodies recognise (antigens mutate)
    > leads to adaptive immune cells not being able to identify the antigens, creating a new disease
  • known pathogens in new populations (settlers to aboriginals)
  • re emergence of known pathogens
47
Q

introduced diseases to indigenous australians

A
  • indigenous australians had no immunity to diseases brought by european settlers
    > epidemic
  • influenza, tuberculosis, measles, smallpox
  • killed upto 90% of people who had contact with the settlers
48
Q

strategies managing disease

A

strategies that:
- restrict movement of people. eg. lockdowns
- help authorities assess risk. eg. testing
- prevent spread from person to person. eg. social distancing, face masks
- management of disease. eg. personal hygiene education, vaccination programs
- manage illness in infected. eg. doctors, hospitals

49
Q

cancer & traditional treatment methods

A

cancer: cells undergo mitosis uncontrollably & produce either a benign, malignant or metastasise (cells break off and move to other parts of body) tumor (mass)
- chemotherapy: cytotoxic drugs
- radiation therapy: directed beams that destroy DNA in cells within the beam
- surgery: removes tumors,

50
Q

immunotherapy

A

activates or suppresses the immune system
- non-specific: stimulate the immune system in general- second line of defence, injection of cytokines
- specific: act on cancer cells directly by stimulating the adaptive immune response

51
Q

specific immunotherapy to treat cancer

A
  • chemotherapy
  • radiation therapy
  • surgery
  • conjugated monoclonal antibodies
52
Q

monoclonal antibodies

A
  • lab grown antibodies produced by a clone of a b cell, specific to a particular antigen.
  • used as a form of immunotherapy to treat cancer (activation immunotherapy) & autoimmune diseases (suppression immunotherapy)
53
Q

producing monoclonal antibodies

A
  1. mice injected with cancer cell antigens
  2. the mice’s B lymphocytes will have an immune response & produce antibodies specific to that antigen.
  3. B cell is isolated and fused with a myeloma (immortal cell), producing a hybridoma (cell with unlimited lifespan)
  4. hybridoma is cloned and produces monoclonal antibodies specific to cancer antigen, which are harvested
54
Q

conjugated monoclonal antibodies

A
  • monoclonal antibodies that have had different things attached to them, such as a radioactive chemotherapy drug or immunosuppressor
  • used to treat cancer
  • target specific cells rather than the whole body
55
Q

monoclonal antibody therapy for autoimmune disease

A

autoimmune disease: where the immune system attacks its own self cells
- suppression immunotherapies can be used to dampen the immune system & reduce its ability to attack self cells
> tumor necrosis factor alpha (TNFA), B & T lymphocyte inhibitors

56
Q

conjugated monoclonal antibodies

A

specific to two things- bind to two different cells and bring them together

Bio 3/4 (4 decks)

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