Specific immune responses Flashcards

1
Q

T lymphocytes (cells)?

A
  • mature in thymus
  • cell-mediated response - involves T cells & body cells
  • ‘cell-mediated’ as T cells only respond to antigens that r presented on cells (APC) - not antigens detached
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2
Q

Antigen Presenting Cells (APC)

A

any cell that present a non-self antigen on surface e.g.
- infected body cells (present viral antigens)
- macrophage/phagocyte (present antigens)
- cells of a transplanted organ (diff shaped antigens)
- cancer cells (abnormal self-cell antigens)
* these trigger cell-mediated response

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3
Q

Cell-mediated response?

A
  • once pathogen has been engulfed & destroyed by phagocyte - antigens positioned on cell surface aka APC
    2. Helper T cells hv receptors on surface - attach on antigens on APC
    3. Once attached ts activates helper T cells to divide by mitosis to replicate & make large nums of clones
    4. Cloned helper T cells differentiate into diff cells:
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4
Q
  1. Cloned helper T cells differentiate into diff cells…
A
  • helper Ts - activate B cells
  • some stimulate phagocytes to perform more phagocytosis
  • some become memory cells for that shaped antigen
  • some become cytotoxic T cells aka killer T cells
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5
Q

Cytotoxic T cells?

A
  • destroy abnormal/infected cells
  • release protein - perforin - embeds in cell surface membrane - makes pore/hole so - any substance can enter or leave cell
  • causes cell death/shrivel/lyse
  • most common in viral infections as - viruses infect body cells
  • body cells sacrificed to prevent viral replication
  • why sore throat when cold - as cytotoxic T cells r destroying infected cells in throat
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6
Q

B lymphocytes (cells)?

A
  • all lymphocytes made in bone marrow
  • B cells mature there too
  • humoral response: Involves B cells & antibodies
  • antibodies r soluble & transport in bodily fluids (aka humour)
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7
Q

B cell activation?

A

*approx 10 mil diff B cells which hv antibodies on surface complementary to 10 mil diff antigens
- antigens in blood collide w complementary antibody on B cell - B cell takes in antigen by endocytosis & presents it on membrane
- when B cell collides w helper T cell receptor - activates B cell - clonal expansion (division) & differentiation (aka clonal selection)…
- B cells undergo mitosis to make large no. Cells - these differentiate into plasma or memory B cells

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8
Q

Plasma and memory B cells?

A
  • plasma - make antibodies
  • Memory - divide rapidly into plasma cells when reinfected with same pathogen - to make large no. antibodies rapidly
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9
Q

Memory B cells?

A
  • can live for decades in body (plasma short lived)
  • divide by mitosis & make plasma cells rapidly if collide w antigen they’ve previously encountered
  • results in large no. Antibodies produced so rapidly that - pathogen destroyed b4 any symptoms can occur
  • active immunity
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10
Q

Primary and Secondary immune response?

A

Pri - first exposure to the antigen/pathogen
- aren’t able to produce many antibodies quickly
- - production of antibodies & memory cells takes a while - the right immune cells to find the pathogen

Sec - 2nd exposure to same antigen - if memory cell collides w complementary antigen - differentiate into more memory cells & lots of plasma very rapidly so-
- lots of antibodies very quickly
- The memory cells are activated and rapidly divide into plasma cells which can then more rapidly produce more antibodies

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11
Q

Antibodies structure?

A
  • quaternary protein structure - 4 polypeptide chains (2 short on outside, 2 on inside)
  • variable region - change shape - complementary shape to specific antigen
  • constant region - alw be the same
  • heavy chain - longer ones in middle
  • light chain
  • antigen binding site - top bit
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12
Q

Agglutination?

A
  • antibodies bind to antigen: Antigen-antibody complex
  • antibodies r flexible so - can bind to multiple antigens to clump tgt
  • makes easier for phagocytes to locate & destroy/engulf more efficieny
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13
Q

Vaccination?

A

involves injection of antigens that have been isolated from a dead/attenuated microorganism
- ts induces a primary immune response in an individual (production of memory cells) w/o them suffering symptoms of the disease

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14
Q

Passive immunity?

A
  • introducing/inserting (monoclonal) antibodies into organism from an outside source
  • pathogen/antigens don’t enter body so - plasma & memory cells not made
  • no long-term immunity
  • e.g. antibodies passed to a fetus thru placenta/thru breast milk to baby
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15
Q

Active immunity?

A
  • involves direct contact w pathogen/antigens - stimulating body’s immune system to produce its own antibodies
    1. Natural active: following infection and creation of body’s own antibodies & memory cells
    2. Artificial active: following introduction weakened version of pathogen/antigens via vaccine
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16
Q

Examples of active & passive immunity - natural and artificial?

A

ACTIVE:
- natural: infection
- artificial: vaccination
PASSIVE:
- natural: maternal antibodies
- artificial: monoclonal antibodies

17
Q

3 Differences between active & passive immunity?

A

active: antibodies secreted by plasma cells
passive: antibodies introduced into body from outside

active: longer term cos memory cells created
passive: short term cos no memory cells created & antibodies eventually break down

active: takes longer to develop
passive: fast acting

18
Q

How do vaccines works?

A
  • introducing antigens stimulates a primary immune response
  • vaccine contains antigen - displayed on APCs
  • soecific helper T cell activates B cell
  • B cell - clonal expansion & differentiation (clonal selection)
  • B cells undergo mitosis - large nums of cells - these differentiate into plasma/memory B cells
  • plasma - make antibodies
  • memory cells divide rapidly into plasma cells when re-infected w same pathogen - make large nums of antibodies rapidly
19
Q

Herd immunity?

A

When a sufficiently large proportion of the population has been vaccinated to make it difficult for a pathogen to spread even to those not immunised

20
Q

Ethical concerns of using vaccines?

A
  • use of animals
  • side effects
  • who should be tested on?
  • should trials only occur in specific countries?
  • should it be compulsory?
  • economical concerns
  • greater food v individual health risks
21
Q

When do vaccines not work?

A
  • pathogen DNA can mutate frequently - if mutation occurs in gene which codes for antigen - shape of antigen will change
  • ineffective as - antibodies can no longer recognise (not complementary to) antigens aka antigenic variability/memory cells hv mem of old antigen shape
22
Q

Features of successful vaccination?

A
  • financially available
  • few side-effects - if any!
  • ways of producing, storing and transporting the vaccine
  • ways of giving (administering) the vaccine properly - may involve training staff
  • be available in sufficient quantities to vaccinate most of the population - herd immunity
23
Q

General - viruses?

A
  • replicate inside cells - - difficult to destroy them w/o harming harming host cells
  • hv diff mechanisms (e.g. respiration/protein synthesis) & no cell wall pores - diff to bacteria
  • antibiotics interrupt/attack organelles of bacteria/reactions so - antibiotics ineffective against viruses
24
Q

HIV structure?

A
  • core: genetic material (RNA) & enzyme - reverse transcriptase - r both needed for viral replication
  • capside - outer protein coat
  • envelope - extra outer layer - made out of membrane taken from host’s cell membrane
  • protein attachments - on exterior of envelope - enables virus to attach to host’s helper T cell
25
Q

HIV general?

A
  • infects person’s blood thru sex, sharing needles, blood transfusion
  • can’t reproduce itself - host cell needed - T helper cells
  • instructs host cell to produce components of new HIV viruses
26
Q

Replication of HIV in helper T cells?

A
  • HIV enters the bloodstream, it circulates around the body
  • Virus binds (using attachment proteins) to receptor proteins (CD4) on the surface of a t-helper cells
  • virus lipid envelope fuses with the cell surface membrane
  • capsid breaks down and this releases the genetic material & enzymes into the cell
  • Reverse transcriptase converts RNA to DNA
  • viral DNA moves into the nucleus through a nuclear pore and is inserted into the host cell DNA by integrase
  • HIV DNA is transcribed into mRNA & then translated into viral proteins
  • These new viral particles are assembled and bud off from the cell surface membrane to infect more cells
  • This destroys T helper cells
27
Q

Retrovirus meaning?

A
  • a group of viruses where virus is able to insert its genetic material into host cell’s DNA using enzyme: reverse transcriptase
28
Q

AIDS?

A
  • AIDS - when replicating viruses in helper T cells interfere w normal functioning of immune system
  • a set of symptoms results from low T helper cells nums due to - rapidly replicating HIV
  • w helper T cells destroyed - host unable to produce adequate immune response to other pathogens so - left vulnerable to infections & cancer