CHAPTER 5: IMMUNITY Flashcards

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1
Q

what are diseases

A
  • a disease is a condition that interferes with the normal functioning of an organism; usually with specific symptoms.
    • can be infectious or noninfectious
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2
Q

what are pathogens

A
  • Most microbes are harmless (non-pathogenic) - only about 1% can cause disease
  • Most pathogens are species-specific and tissue-specific
  • Pathogens are agents that cause diseases in their hosts
  • can be extracellular → pathogen in the body but not in the cells yet (innate response)
  • can be intracellular → pathogens in the cells (adaptive response)
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3
Q

cellular vs non-cellular pathogens

A
  • cellular: made of cells and can reproduce independently
    • bacteria, parasites (worms), fungi, protozoa
  • non-cellular: not made of cells and cannot reproduce independently → need the cells of the host to reproduce (hijack)
    • viruses, prions
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4
Q

what are antigens

A

antigens are substances that cause/stimulate an immune response

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5
Q

self vs non-self antigens

A
  • Self-antigens: antigens on cells that are recognised by self-receptors as being part of the same body
    • tolerated by the immune system
  • Non-self antigens: antigens that do not belong to the body’s own cells
    • attacked by immune system
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6
Q

distinguishing self from non-self

A
  • plasma membrane of this immune cells carries:
  • self-antigens that identify this immune cell as ‘self’
  • cell surface receptors for self-antigens so that this cell can identify and not attack other body cells
  • cell surface receptors for foreign antigens so that the immune cell can identify foreign material and signal other immune cells to eliminate it
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7
Q

MHC I vs MHC II markers

A
  • both are located on the outside of cells, anchored to the cell membrane and are specific to individuals.
  • MHC-I markers are present on all nucleated cells
    (not red blood cells) of the body and present the peptide fragments from inside the cells
    • they signify if a cell is ‘self’ or ‘non-self’
    • if the correct MHC-I marker is not detected, immune cells will cause it to undergo apoptosis.
  • MHC-II markers are only found on specific cells in the immune system such as macrophages, dendritic cells, and B lymphocytes
    • all involved in antigen presentation → present the antigens from outside the cell.
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8
Q

bacteria

A
  • prokaryotic microbes and their genetic material is double-stranded DNA
  • If bacteria multiply in areas they are not normally found they can cause disease
  • Intracellular and extracellular
  • Symptoms of bacterial infection are often caused by the toxins the bacterium produces
    Bacteria can cause disease in humans if:
    1. They can enter a person who can act as a host.
    2. They have the capacity to reproduce within the host.
    3. They act adversely on tissues in their host (exotoxins, adverse enzyme production)
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9
Q

protozoans

A
  • single-celled, eukaryotes
  • infection by ingestion of cysts by sexual transmission or insect vectors
  • able to multiply in humans, enabling them to survive in a human host while causing disease.
  • symptoms: blood, gut and lymphatic system
    • Eg. Malaria – bites of mosquitos
    • Ingesting contaminated food
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10
Q

fungi

A
  • eukaryotes
  • grow from the tips of filaments (hyphae) that make up the bodies of the organisms (mycelia)
  • opportunistic pathogens - immune system is weak
  • usually external or skin infections
    • Eg. Candida albicans - Thrush (oral
      candidiasis)
    • Athletes food – tinea (Trichophyton spp.)
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11
Q

parasites (worms)

A
  • (not microbes) can be seen with the naked eye
  • transmitted via soil contaminated with human faeces that contains eggs of those worms
    • Eg hookworm, roundworms, whipworms
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12
Q

viruses

A
  • comprise of nucleic acid (DNA or RNA) surrounded by one or more coats of protein.
  • replicate only within host cell
  • viruses cause disease by killing body cells
  • to make more viruses, a virus takes over a host cell and uses it as a ‘factory’
  • release of viral particles from an infected cell may be by budding or by cell lysis
  • infected host cell ‘explodes’ as its plasma membrane disintegrates and viral particles are released into the extracellular fluid from where they can infect other cells.
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13
Q

what is the immune system

A

the body system that helps resist infections and disease through specialised cells

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14
Q

3 levels of the immune system

A

INNATE - present from birth, no immunological memory, not acquired

  • the first line of defence
    • innate
    • non-specific
    • skin, stomach acid, etc.
  • the second line of defence (hasn’t infected cells yet)
    • innate
    • non-specific
    • macrophages, inflammation, complement proteins
    • the non-specific cellular and molecular responses to pathogens that have breached the first line of defence and have entered the body.
    • The innate immune response is nonadaptable, and does not change during an individual’s lifetime.

ADAPTIVE - more targeted to a specific pathogen
- third line of defence
- acquired (learns and has memory)
- specific
- B cells, T cells, antibodies
- takes time to develop

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15
Q

first line of defence

A
  • physical barriers act to prevent the entry of pathogens
  • chemical barriers act to inhibit the growth or development of pathogens and/or act to destroy pathogens
  • microbiota barriers act to prevent the growth or colonisation of microorganisms that may be pathogenic.
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16
Q

first line of defence: physical barriers

A
  • intact skin
  • skin microbiome
  • mucus: traps and prevents entry of pathogens
  • earwax
  • nostril hair
  • acidic environment - digestive, reproductive, and urinary systems
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17
Q

first line of defence: chemical barriers

A
  • destroys pathogens on the outer body surface, body openings, and on inner body linings
  • sweat, mucus, tears, saliva (all have enzyme lysozyme that kills pathogen)
  • stomach acid - kills pathogens
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18
Q

first line of defence: microbiological barriers

A
  • presence of normal flora
  • non-pathogenic bacteria in regions of the body
  • inhibits the growth of pathogenic microbes
  • also called “commensal bacteria”
  • gut contains many microbes [mainly bacteria] which exist in a “mutualistic relationship” with the person.
  • prevent the growth of colonies of other species of bacteria by outcompeting them for nutrients and adhesion sites, and secreting antimicrobial chemicals
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19
Q

first line of defence: plant barriers

A
  • plants do not have an immune system comparable to animals, but they have developed structural, chemical and protein-based defences
    • cuticle: waxy covering - prevents penetration and virus and bacteria entering
    • thick bark
    • leaf orientation (horizontal or vertical) - vertical is less susceptible to pathogens
    • thorns and spikes
    • antimicrobial or antifungal compounds (plants can naturally make this)
    • formation of galls
      • growing ‘gall’ tissue around the area containing the infective agent to prevent spread to other areas (containing the pathogen)
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20
Q

second line of defence

A

if the preventative strategies don’t keep the pathogen out, foreign antigens need to be recognized

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21
Q

cells of the immune system

A
  • immune system cells are white blood cells → leukocytes (another name for white blood cells) made in bone marrow
  • each has a specific role in defending the body from pathogens and infectious disease
  • involved in innate immunity
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22
Q

dendritic cells (phagocyte)

A
  • found in tissues
  • reside in and patrol the skin and mucosal surfaces
    • can migrate to lymph nodes
  • engulf and destroys pathogens by phagocytosis
  • antigen-presenting cells that can activate an adaptive immune response
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23
Q

what are phagocytes

A
  • phagocytes (macrophages, monocytes, neutrophils, dendritic cells)
  • do not recognize specific antigens but instead recognize patterns on antigens
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24
Q

macrophages (phagocyte)

A
  • found in tissues
  • identify and eliminate pathogens by phagocytosis
  • antigen-presenting cells that can activate the adaptive immune system
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25
Q

eosinophils

A
  • present in the respiratory, gastrointestinal and urinary tracts
  • assist in defending against larger multicellular parasitic agents
  • granules with toxic chemicals and induce the degranulation of histamines from mast cells
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26
Q

neutrophils (phagocyte)

A
  • found in blood
  • first cells to arrive at the infection site
    • attracted to foreign materials by chemical signals
  • engulf and destroy pathogens by phagocytosis
  • granules in cytoplasm contain antimicrobial agents or enzymes to assist with destruction
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27
Q

process of phagocytosis

A
  • the phagocytes recognize the microbe via a receptor
  • the phagocyte engulfs the microbe via endocytosis
  • the vesicle containing the microbe fuses with a lysosome
  • the lysosome (organelle) empties its digestive enzymes into the vesicle → lysosomes have a lot of digestive enzymes
  • the enzymes digest the microbe
  • the particles are released from the phagocyte
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28
Q

natural killer (NK) cells

A
  • found in blood/lymph
  • kill virus-infected cells
  • attack cells lacking self markers - missing/abnormal MHC markers
  • have granules filled with potent chemicals
  • NATURAL KILLER CELL ACTION: DEGRANULATION
    • when an NK cell recognizes an abnormal cell, it releases proteases (enzymes) and perforin
    • perforin punches holes in the cell membrane, allowing the proteases to enter
    • these trigger apoptosis (destroys it from the inside)
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29
Q

mast cells

A
  • found in tissue - close to the external environment (eg. surface of the skin)
  • mediate inflammatory response
  • contains chemicals in granules - cytokines, histamine
    • histamines increase permeability - in terms of blood vessels
    • cytokines attracts other immune cells
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30
Q

humoral innate immunity

A
  • immune response in the ‘humors’ → body fluids
  • eg. lymph, blood
    • complement proteins
    • interferons
    • (extracellular body fluids)
    • soluble/dissolved in fluid eg. blood, lymph
31
Q

complement proteins

A
  • inactive enzymes in blood that complement the function of immune cells
  • activated when they make direct contact with the molecules on the surface of a pathogen
  • complement proteins activate other complement proteins to form a cascade (like a domino effect)
  • complement proteins can cause inflammation (acts as chemotaxis), enhance phagocytosis or cause lysis

works against both cellular and non-cellular pathogens

32
Q

opsonisation (action of complement proteins)

A
  • makes pathogens more susceptible to elimination by phagocytosis
  • coat the surface of pathogen cells and the phagocytes have receptors for the complement proteins (bind to the opsonised microbe)
33
Q

chemotaxis (action of complement proteins)

A
  • movement of cells in response to a chemical stimulus
  • small complement peptides that diffuse from the pathogen surface act as chemical signals
  • attracting immune cells involved in the inflammatory response to the site of the infection
34
Q

lysis (action of complement proteins)

A
  • membrane attack complex (MAC) forms on the plasma membrane of the pathogen due to complement proteins
  • the MAC inserts into the plasma membrane of the pathogen, producing a pore
  • this allows fluid to enter and causes the pathogen cell to swell and burst
35
Q

interferons

A
  • a group of cytokines (signalling proteins)
  • virally infected cells release interferons to prepare neighbouring cells for a possible ’attack’
  • the interferon secreted acts as warning signals to nearby cells
    • signal change in plasma membrane making entry of virus more difficult (make PM less fluid)
    • signals neighbouring uninfected cells to prepare to destroy RNA to reduce protein synthesis
    • signal neighboring infected cells to undergo apoptosis
    • activates immune cells such as NK cells
36
Q

inflammation - major weapon of innate immunity

A
  • reaction to an infection/injury/damaged tissue/pathogen
    • localised to the site
  • prevent the spread of antigen, removes the pathogen and dead cells, restores the tissue to normal (healing)
  • results in heat, pain, swelling and redness
37
Q

process of inflammation

A
  • vascular stage → blood cells
  • cellular stage → immune cells
  • resolution → normal state restored and inflammation is stopped
38
Q

vascular stage

A
  • damaged cells release cytokines → attracts neutrophils
  • mast cells release histamines → causes capillaries to become permeable (leaky) and wider (vasodilation)
  • vasodilation: increases blood flow to damaged area and the increased blood flow produces heat and redness
  • permeable: protein-rich fluid (exudate) can escape from capillaries to the infected region
    • the exudate causes swelling and the swelling causes pressure on surrounding tissues, stimulating nerve endings→ cause pain
39
Q

cellular stage of inflammation

A
  • phagocytes are attracted to the site by cytokines → phagocytose antigen
  • complement proteins opsonise pathogens → phagocytosis can occur
  • platelets travel to the site to block wound → important for clotting
  • pus indicates that this stage is occurring
    • consists of mainly dead phagocytic cells and other immune cells, dead tissue, dead pathogens
40
Q

resolution stage

A
  • occurs when the tissue is returned to normal state → infection is under control
  • the release of cytokines stop and anti-inflammatory cytokines are released
  • resolution occurs when the antigen is removed from the site of infection
  • if resolution does not occur, chronic inflammation may occur
41
Q

lymphatic system

A
  • transport network
  • consists of
    • lymph
    • lymph vessels
    • lymph organs
  • production and maturation of immune cells
  • allows for the process of antigen recognition by T and B cells
42
Q

roles of components of lymphatic system

A
  • thymus: maturation of T cells
  • bone marrow: maturation of B cells (B+ T both made in bone marrow but B stays there and T cells move through the lymphatic system to the thymus)
  • lymph nodes: meeting, activation and response
  • lymph vessels connect lymphoid organs (transport)
  • spleen: filters blood
    • contain B, T, dendritic cells and macrophages
    • activation of B and T cells
43
Q

primary lymphoid organs

A
  • primary tissue where B and T cells are made
  • bone marrow
    • source of pluripotent stem cells - leukocytes originate (lymphocytes: B and T cells)
    • the site of maturation of B cells
  • thymus
    • thymus is the site where T cells mature after being released from the bone marrow
44
Q

secondary lymphoid organs

A
  • mature B and T cells are activated
  • where antigens presentation occurs (also filter lymph - the fluid)
  • lymphoid organs contain lots of lymphocytes → B and T cells
  • spleen
    • filters blood → clearing of bacteria and/or viruses and worn-out red blood cells
    • contains T and B cells
    • contained macrophages and dendritic cells
  • lymph nodes
    • main site of antigen recognition → leading to the adaptive immune response
45
Q

lymph nodes

A
  • small bean-shaped structures
  • the site of ANTIGEN RECOGNITION in which T and B lymphocytes come into contact with their specific antigens → adaptive immune response occurs
  • swell when infections occur → number of B and T cells in the lymph nodes increase → this produces the so called swollen glands
46
Q

maturation of lymphocytes

A
  • activated by meeting their complementary antigens
  • antigens presented by macrophages or dendritic cells
  • B and T lymphocytes have receptors for only ONE SPECIFIC ANTIGEN
  • B cells make antibodies to eliminate pathogens (antibody-mediated)
  • T cells eliminate infected or diseased cells (cell-mediated)
47
Q

how is adaptive immune response initiated

A
  • pathogen enters (first line of defence breached)
  • meet at the entry point by phagocytes that engulf and eliminate’
  • some of the digested fragments of the antigen are displayed on the MHC II receptors on the surface of dendritic cells or macrophages
  • APCs migrate to the lymph nodes and present the antigen to the T helper cells that carry complementary receptors for the antigen
  • T helper cells release cytokines
  • initiates the adaptive immune response
    • humoral B cells
    • cell-mediated T cells
  • NEUTROPHIL IS NOT AN ANTIGEN PRESENTING CELL BUT CAN UNDERGO PHAGOCYTOSIS
48
Q

role of helper t cells

A
  • only activated by antigen-presenting cells that present antigen on the MHC II marker
  • once active, clone and secrete cytokines which
    • help activate cytotoxic T cells (Tc)
    • help activate B cells into plasma cells
    • help activate macrophages to remove antibody-coated pathogens by phagocytosis
49
Q

how does antigen presentation occur

A
  • pathogen undergoes phagocytosis
  • antigen fragment is presented on the MHC II molecule to helper T cells
  • helper t cells have a receptor
50
Q

what is adaptive immunity

A
  • adaptive immunity involves a specific response against a specific pathogen → with memory retained for future infections
  • this immune response is usually only required if an infection is not cleared by the innate response
  • specificity: adaptive immune cells (B and T cells) have unique receptors that recognise specific antigens
  • immunological memory: remember antigens after primary infection → to enable a more rapid and stronger response in case of future infections
51
Q

adaptive cell mediated response

A
  • intracellular pathogens
  • T cells deliver the cell-mediated immune defences that include the direct elimination of the pathogen-infected cells and other abnormal cells such as cancer cells
  • are activated by antigen-presenting cells
  • stimulated by Th
    • memory T cells
    • cytotoxic T cells
52
Q

humoral response

A
  • extracellular pathogens
  • B cells deliver the humoral immune defences by
  • secreting antibodies that bind to surface antigens on pathogens and label them for elimination → antibodies also bind to soluble toxins
53
Q

action of cytotoxic T cells

A
  • cytotoxic T cells recognise virus-infected cells and can also recognise abnormal proteins
    • eg. DNA mutations in cancer cells which often results in abnormal MHC-I markers
    • this means cytotoxic T cells can target and eliminate cancer cells.
  • once activated, T cells recognise the presence of foreign antigens on the surface of body cells by intracellular pathogens
  • can be initiated by APC presents antigen using MHC II
    • use T helper cells
  • cytotoxic T cells proliferate, producing activated cytotoxic T cells and memory T cells through clonal selection and expansion
  • memory T cells retain memory of antigens met previously
  • clonal selection: Tc cell binds with its antigen in lymph nodes
  • clonal expansion: the activated Tc cells divide into many identical copies (clones) all having identical antigen binding receptors
54
Q

steps in cell-mediated immunity

A
  • APCs display foreign antigen on MHC II marker to specific helper T cells usually within lymph node
  • helper T cells undergo clonal selection and expansion
  • interleukins (type of cytokine) are secreted by helper T cell to stimulate immature T cells
  • upon stimulation by cytokines release by Th cells, cytotoxic T cells proliferate and produced activated cytotoxic T cells and memory T cells through clonal selection and expansion
  • cytotoxic T cells destroy the cells through apoptosis
55
Q

apoptosis by cytotoxic T cells

A
  • if a cytotoxic T cell (has toxic granules) recognises an infected cell it
    • releases perforin (a protein that inserts into the plasma membrane and creates pores)
    • enzyme (granzyme B) enter via the pore and trigger apoptosis from within the cell
    • this ensures that the virus cannot spread
    • similar to the action of NK cells but cytotoxic T cells are specific for certain antigens and form memory cells
56
Q

B lymphocytes role in humoral immunity

A
  • B lymphocytes (cells) are covered in receptors → known as antibodies
    • antibodies are membrane-bound or free
    • B cells are ‘selected’ when they find an antigen (extracellular pathogen) complementary to the antibody
    • most need to be activated by Th cells
    • some become memory B cells
    • most become plasma cells
57
Q

clonal selection and expansion in B cells

A
  • clonal selection: B cells bind with its specific antigen in lymph nodes
  • clonal expansion: the activated B cells divide into many identical copies (clones) all having identical antigen-binding receptors
58
Q

memory cells vs plasma cells

A
  • memory cells:
    • not active
    • ‘lifelong’
  • plasma cells:
    • active
    • short-lived
    • secrete antibodies
    • each plasma cell can only produce one type of antibody.
59
Q

events of humoral immunity

A
  • an antigen gains entry to the body for the first time
  • comes into contact w/ many naive B cells in the lymph nodes that don’t recognise it
  • eventually, the antigen meets a B cell that can recognise and binds to it
    • called clonal selection
  • helper T cells that have also bound to the antigen release cytokines to activates the selected b cell- the binding of antigen to T helper cells activate the selected B cell to differentiate and proliferate into B plasma cells and B memory cells.
    • results in the production of a large number of B cells w antigen-binding receptor antibodies
    • clonal expansion
  • plasma cells secrete soluble antibodies against the specific antigen
  • memory B cells remain in the lymphoid tissue after the infection has resolved
    • initiate immune responses more rapidly and stronger upon re-exposure to the same antigen
    • produces large amounts of the specific antibody
60
Q

structure of antibodies/immunoglobulins

A
  • they are antigen-binding proteins made by plasma B cells
  • made of 4 polypeptide chains → 2 heavy and 2 light chains (quaternary structure) → constant region (doesn’t vary between antibodies of the same class)
  • each antibody has 2 identical specific antigen-binding sites on both sides of the antibody
  • variable region is the antigen binding site → differs between antibodies
    • located at the end of each arm of the Y shaped molecule
    • the variable region gives antibody its specificity for binding antigen
  • each antibody can only bind to one specific antigen
  • there are billions of antibodies each w a different antigen-binding site
61
Q

classes of antibodies

A
  • IgG: main antibody in blood
  • IgM: first antibody to appear and provides defence until sufficient IgG is formed
  • IgA: attaches to the surfaces of mucous membranes
  • IgE: stimulates the release of histamine and other chemicals that cause allergies
  • IgD: antibody found on B cells
62
Q

action of antibodies

A
  • antibodies do not directly eliminate antigens
  • they can:
    • bind to antigens and form a coating that neutralises pathogens by blocking their receptors so that the pathogens cannot attach to healthy body cells and infect them and stop them from functioning neutralisation (common)
  • bind to surface antigens to target them for phagocytosis opsonisation
    • bind to surface antigens to target them for lysis by complement proteins
    • antibodies bind to surface antigens on pathogens to form antigen-antibody complexes → causing them to clump together and be more visible to the immune system agglutination (common)
    • precipitation —antibodies bind to soluble antigens, making them insoluble. This causes them to precipitate out of the solution, creating a solid that is much more visible to the immune system. This occurs due to the cross-linking between antigens and antibodies.
    • inflammation —antibodies can trigger the release of histamine, causing inflammation. They also activate a complement cascade.
    • PIANO acronym
63
Q

memory B cells

A
  • memory B cells remain in the lymphatic tissue to remember the antigen for future infections
  • they initiate immune responses more rapidly and strongly upon re-exposure to the same antigen, producing large amounts of the specific antibody.
  • antibody levels peak in the primary response at about day 14 and then begin to drop off as the plasma cells begin to die (low and short-lived)
  • there are more memory cells than there were naive B cells for the primary response
    • so secondary response: more plasma cells are generated and antibody levels are consequently 100-to-1000 fold higher
64
Q

what are allergens

A
  • antigens are substances that cause/stimulate an immune response → doesn’t have to be biological (wood splinter)
  • pathogens are agents that cause disease in their response
  • allergies are caused by an immune response to allergens (antigens)
  • allergic reaction is an abnormal overreaction when exposed to an allergen
    • usually harmless → some are hypersensitive
  • involves the cells of both the innate and adaptive immune system
  • not all antigens are pathogens
  • allergies are caused by an immune system response to allergens (antigen ) eliciting an allergic response
65
Q

what is an allergic reaction

A
  • a reaction to a normally harmless substance
  • the substance that causes an allergic response is an allergen (not antigen)
  • key players in allergic reaction:
    • mast cells
    • antibodies → immunoglobulin E (IgE) - overproduction of IgE antibodies causes an allergic response
66
Q

steps in an allergic response

A

first exposure:

  • allergen (eg. pollen) enters into the bloodstream (first exposure)
  • B cells- specific to the allergen (bc extracellular) differentiate into plasma cells and make antibodies
  • IgE antibodies attach to mast cells
  • called ‘PRIMED’ → ready to respond to the allergen

secondary exposure:

  • mast cell is primed with IgE antibodies specific for that allergen
  • the allergen binds to antibodies on mast cells
    • cross-links form→ more than one antibody binds with the allergen (activates more than one antibody)
    • histamines will only be released when there is a crosslink (when allergen binds to j one antibody, histamines aren’t stimulated - no inflammation)
  • histamine is released from the mast cell
  • cytokines are released → attracting more immune cells
  • an allergic reaction occurs
    • increased blood flow
    • increased permeability of blood vessels
    • sustains and increases reaction (more histamine can be released)
67
Q

how can you be immune from a disease

A

when we have antibodies against an antigen → we won’t develop the disease

68
Q

sources of antibodies

A
  • active: own immune system produces long-term immunological memory (produces own antibodies and makes memory B cells)
    • secondary response is more enhanced due to memory
    • long-lasting
    • more effective
    • immunity develops over weeks
    • eg. infected, vaccine
  • passive: external source, short term, NO immunological memory (made externally so memory B cells aren’t produced) → quicker response eg. get bitten by snake, antivenom injected
    • short lasting
    • less effective
    • immunity is immediate
    • eg. from mother, injected vaccine
69
Q

means of gaining immunity

A
  • can be natural or artificial
  • natural immunity:occurs without deliberate intervention
    • infection, mother-child
  • artificial immunity: is created by deliberate intervention and exposure
    • vaccine, injection of antibodies
70
Q

active immunity

A
  • natural
    • infection by pathogen-causing agent
    • antibodies form with identical antigen binding sites that bind to the antigens
    • pathogen destroyed by high amounts of antibodies
    • formation of memory cells
  • artificial
    • deliberate introduction of a disabled pathogen
    • eg. injection
    • the adaptive immune response is activated to produce the antibodies
71
Q

passive immunity

A
  • natural
    • receives antibodies from a natural source
    • eg. breastfed milk →colostrum via the placenta, IgG
  • artificial
    • provided by injection of antibodies such as antivenom or antitoxins
    • eg. clostridium tetani, rabies virus, antivenom (after pathogen enters the body, these are injected)
72
Q

tonsils

A
  • Have specialised cells called microcells that can trap antigens and present them to macrophages or dendritic cells [APCs] which will then engulf them and take them to the lymph nodes 7 present them to the B & T lymphocytes
73
Q

infection vs disease

A

Infection is the invasion and growth of a pathogen in the body
Disease is a condition that impairs the normal functioning of an organ, structure or system of an organism

74
Q

how does a virus hijack a cell

A
  • Virus adheres and inject viral nucleic acid or is taken up by cell.
  • Viral nucleic acid moves to nucleus where it is transcribed.
  • Viral mRNA is then translated (USES CELL’S ORGANELLES TO REPRODUCE)
  • Viral protein is then packaged
  • cell bursts releasing the viruses