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Biology 3/4 > chapter 7&8 (antigens, immunity & diseases) > Flashcards

chapter 7&8 (antigens, immunity & diseases) Flashcards

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1
Q

self antigens

A
  • located on the surface of cells
  • marked as ‘self’ so immune system does not attack
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2
Q

MHCI

A
  • major histocompatibility complex
  • expressed on all cells except those without a nucleus (e.g red blood cells)
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3
Q

MHCII

A
  • major histocompatibility complex
  • found on specialised cells of the immune system
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4
Q

non-self antigens

A
  • immune system reads as ‘foreign’ and is activated to kill it
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5
Q

cellular pathogens

A
  • have cell structure and are living organisms
    BACTERIA: disease through enzymes and toxins effecting functions in cell
    FUNGI: yeast and mould organisms
    PARASITES: invertebrate (eggs, larval)
    PROTOZOA: free living, parasitic, inhibits functions
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6
Q

non-cellular pathogens

A

VIRUSES: composed of genetic material in protein coat, uses host cells to replicate (unable to itself)
PRIONS: abnormally folded proteins which causes other miss folding, only occurs in mammals and affects the brain

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7
Q

allergies & allergens

A

ALLERGIES: overreaction to the presence of an allergen
ALLERGEN: a non-pathogenic antigen that triggers an allergic reaction (inflammatory response, breathing issues)

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8
Q

first line of defence plants
(non-specific/innate)

A
  • physical- prevent pathogens from physically entering
    (e.g bark, galls, closing of the stomata)
  • chemical- production of chemicals which are harmful to pathogen
    (e.g phenols (repel/kills), defensins(toxic))
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9
Q

first line of defence animals
(non-specific/innate)

A
  • physical - e.g skin, cilla/hair like structures, mucous secretions
  • chemical - e.g acidic sweat, stomach acid & antibacterial parts of earwax
  • microbiological - prevents growth of pathogenic bacteria
    (e.g normal flora on skin and gastrointestinal tract)
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10
Q

second line of defence cellular components
(non-specific/innate)

A
  • natural killer cell: destroys infected/abnormal cells with insufficient MHCI markers
  • mast cells: causes inflammation through release of histamine
  • eosinophils: releases toxic chemical mediators to destroy invading pathogens
  • phagocytes: cells that engage phagocytosis (engulfing via endocytosis)
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11
Q

phagocytes

A
  • neutrophils: phagocytosis of pathogens
    macrophage/dendritic cells: phagocytosis of pathogens and the antigen presentation within the adaptive immune system (APC)
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12
Q

second line of defence non-cellular components
(non-specific/innate)

A

-interferons: causes changes to neighbouring cells that make them less susceptible to infection
-complement proteins: aids in the destruction of pathogens via opsonisation (surrounded), chemotaxis (attraction of phagocytes), lysis (MAC, swell/burst)
-fever: abnormally high body temperature to kill pathogens

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13
Q

inflammatory response

A

-initiation: damage, introducing pathogens, mast cells degranulate and release histamine
-vasodilation: histamine travels to blood vessels, widens increasing blood flow and causes swelling, redness & warmth
-migration: number of innate immune components leave bloodstream and enter injury site (PUS: is caused by increase blood flow and immune cell activity/dead cells)
- this continues until site is cleared

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14
Q

third line of defence
(specific/adaptive)

A
  • APC take antigen to t-helper cell and t-helper cell is activated
  • t-helper cell release cytokines
  • cytokines and pathogens(B) active T and B cells
  • once activated they remember the pathogen
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15
Q

humoral immunity (external)

A
  • COLONAL SELECTION: a pathogen with complementary antigen to the B cell bind, a t-helper cell also complementary recognise the selected B cell and secrete cytokines
  • COLONAL EXPANSION: the B cell replicated and many copes are formed
  • DIFFERENTIATION: differentiates into b-memory cells and plasma cells
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16
Q

antibodies (released from plasma cells)

A
  • consists of four polypeptide chains (two heavy chains/long and two light chains/short)
  • joined by disulphide bond
  • variable and constant region
    five types: IgA, IgD, IgE, IgG, IgM
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17
Q

key functions of antibodies

A
  • neutralisation: block site used to attack host cell & block toxins
  • agglutination: bind together with antigens of pathogens to make a larger complex for phagocytes to recognise and destroy
  • opsonisation: antibody binds to pathogen to easily phagocytose
  • activation of complement proteins: antibodies attach to surface and facilitate activation
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18
Q

cell-mediated immunity (internal)

A
  • COLONAL SELECTION: naive T cell complementary to the antigen presented will bind with APC at the same time as the t-helper cell, naive T cell is now selected, t-helper cell releases cytokines
  • COLONAL EXPANSION: the cytokines released stimulate the T cells to replicate and form copies
    DIFFERENTIATION: differentiates into t-memory cells and cytotoxic-t-cells
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19
Q

cytotoxic-t-cells

A
  • arrives at site of infection
  • cytotoxic-t-cells contains receptor specific to foreign antigen
  • finds the abnormal cell and binds the complementary MCHI complex
  • chemicals (perforin) are secreted by the cytotoxic-t-cells and induce apoptosis
20
Q

immunological cell memory

A
  • b-memory cells form new antibody producing plasma cells when antigens match their receptors
  • t-memory cells rapidly turn into t-helper cells and cytotoxic-t-cells from stimulation from the APC
21
Q

primary lymphoid tissue

A
  • where it is produced and matured
    BONE MARROW: B lymphocytes remain in bone marrow to mature
    THYMUS: T lymphocytes travel to the thymus to mature
22
Q

secondary lymphoid tissue

A
  • where it is stored
  • lymph noes, spleen, tonsils
  • when APC travel to the lymph nodes to activate T and B cells results in a large number of cells and therefore swelling of lymph nodes
23
Q

lymphatic system as transport network

A
  • DRAINAGE: after injury liquid from blood vessels can leak, the fluid is drained by the lymphatic capillaries
  • FLOW: capillaries join together to form vessel that re full of lymph and get pushed towards lymph nodes
  • SURVEILLANCE: fluid arrives at lymph nodes via afferent vessel, antibodies and cytotoxic-t-cells exit via efferent vessels
24
Q

natural active immunity

A
  • own immune system creating antibodies and memory cells specific to that pathogen
  • antibodies from individual immune system
    e.g getting chickenpox and then being immune afterwards
25
Q

natural passive immunity

A
  • acquires antibodies from natural, non medical sources
  • external source of antibodies
    e.g antibodies from placenta/breast milk
26
Q

artificial active immunity

A
  • own adaptive immune system produces antibodies and memory cells due to medical intervention
  • antibodies from individual immune system
    e.g vaccines
27
Q

artificial passive immunity

A
  • acquires antibodies from external source via medical intervention
  • external source of antibodies
    e.g anti-venom
28
Q

primary and secondary vaccination

A
  • PRIMARY: antibodies and memory cells formed, diminishes quickly
  • SECONDARY: memory cells recognise the vaccine, large immune response, resulting in large long-lasting immunity
29
Q

herd immunity

A
  • protection against disease when a high percent of population (approx. 70%) is immune to the disease
  • often achieved through vaccination
  • helps prevent the spread
30
Q

contagious & virulent

A
  • contagious: how easily it is transmitted between people
  • virulent: how severe is the disease the pathogen causes
31
Q

emerging & re-emerging

A
  • emerging: diseases that have no occurred in humans before
    e.g COVID-19, influenza
  • re-emerging: once were major public health problems and then declined but once again are becoming a problem
    e.g ebola, measles, malaria
32
Q

epidemic & pandemic

A
  • epidemic: specific population and specific location
  • pandemic: spread to different countries and/or continents

(endemic - one specific area)

33
Q

factors contributing to emergence and re-emergence of diseases

A
  • evolution of organisms
  • globalisation and travel
  • exposure of humans to animals
  • increasing human population
  • changing technology
  • insufficient vaccination
34
Q

lack of immunity in indigenous population

A
  • europeans would have encountered the disease in their childhood, some form of natural active/passive immunity
  • Indigenous Australian’s had no immunity and therefore were more likely to severely contract the disease
35
Q

lack of knowledge and experience

A
  • Indigenous understood how to treat their own diseases but not the new european diseases
  • medicine was often prevented and therefore there was no treatment
36
Q

disruption due to colonisation

A
  • access to food was redistricted and denied
  • forced into camps, and infection where heightened due to close proximity
37
Q

methods of identifying pathogens

A
  • physical: microscopes
  • phenotypic: selective media
  • immunological: serology (presence of antibodies or antigens
  • molecular: whole genome sequencing (provides info)
38
Q

modes of disease transmission

A
  • airborne transmission
  • droplet transmission
  • direct physical contact
  • indirect physical contact (food/mosquitoes)
  • faecal-oral transmission
39
Q

controlling disease transmission

A
  • prevention (hygiene, PPE, vaccination, lockdown)
  • screening (routine testing)
  • quarantine and isolation
  • identification (identify pathogen)
  • control transmission (mitigate)
  • treating the infected (use of medication such as antiviral)
40
Q

immunotherapy

A
  • a form of medical treatment that modulates the functioning of the immune system in order to treat disease
  • ACTIVATION IMMUNOTHERAPIES: induce or amplify an immune response
  • SUPPRESSION IMMUMOTHERAPIES:
    prevent or reduce an immune response
41
Q

examples of immunotherapies

A
  • CAR-T therapy: modification of t cells to destroy cancer cells
  • dendritic cell therapy: activation of lymphocytes kill any tumour antigens
42
Q

monoclonal antibodies and production

A
  • laboratory-made proteins that can be used to treat a number of different diseases
    STEPS:
  • cancer cell antigen identified
  • vaccination/injection of mouse
  • cells/extraction of mouse cells
  • fuse of cells with myeloma cells to form hybridomas cells
  • selection of hybridomas cells
  • collection and purification of antibodies
43
Q

two types of monoclonal antibodies

A
  • naked monoclonal antibodies (nothing attached)
  • conjugated monoclonal antibodies (drugs/material attached)
44
Q

monoclonal antibodies against cancer and autoimmune disease

A

CANCER
- antibody-dependent cell-mediated cytotoxicity: (bind to cancer cells and use NK cells)
AUTOIMMUNE DISEASE
- cytokine inhibition: (bind and inhibit cytokines to reduce immune response)

45
Q

traditional cancer treatment

A
  • chemotherapy and radiotherapy
  • many other cells are suffered by these treatments causing hair loss, and nausea
46
Q

article info

A
  • smallpox was a pandemic
  • infected the lymphatic system
  • was spread through contact with scabs or contamination
  • using inoculation (deliberately infected with scabs) if they survived they gained immunity
  • smallpox pus was injected under the skin if they survived they gained immunity
  • smallpox disease could withstand most and stayed viable
  • with the cowpox virus the vaccine was created (less symptoms compared to smallpox, then gain immunity)
  • smallpox was eradicated in 1977

Biology 3/4 (10 decks)

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