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9700 > IMMUNITY > Flashcards

IMMUNITY Flashcards

1
Q

Immunity

A

Protection against disease

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2
Q

immune system

A

The body’s defense system

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3
Q
A
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4
Q

Lines of Defences Against Diseases

A

To prevent infectious diseases from entering and spreading

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5
Q

1) First line of defence

A

External, non-specific

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6
Q

2) Second line of defence

A
  • Internal, non-specific immune
    response
  • Involves phagocytes
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7
Q

3) Third line of defence

A
  • Internal, specific immune response
  • Involves lymphocytes
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8
Q

Both non-specific and specific defences work

A

together to protect the
body against diseases

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9
Q

Antigens

A

In general, antigens are macromolecules on cell surfaces
* E.g. protein, glycoprotein, glycolipid, polysaccharides etc.

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10
Q

2 TYPES OF ANTIGENS

A

Self and Non-self

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11
Q

Non-self antigens =

A

macromolecules that activates an immune response
Macromolecules are found on…
– foreign materials’ surface (e.g. pathogen, allergen)
– surface membrane of infected host cells
→Stimulates production of antibodies

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12
Q
A

non self antigen

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13
Q

self antigens AKA

A

cell marker

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14
Q

self antigens

A
  • Macromolecules on cell surface membranes of host cells
  • Cell surface antigens do NOT trigger body’s immune system
  • No antibodies are produced
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15
Q

when we say antigen in general

A

we are usually
referring to NON-self antigen though

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16
Q

Immune response =

A

the body’s immune reaction towards
non-self antigens
Involves WBCs that made in bone marrow

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17
Q

2 types of WBS

A

phagocytes and lymphocytes

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18
Q

phagocytes in _ defence

A

non specific

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19
Q

lymphocytes in _ defence

A

specific

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20
Q

2 types of phagocytes

A

Neutrophils
* Monocytes
→ which mature into macrophages

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21
Q

2 types of Lymphocytes

A

B-lymphocytes
* T-lymphocytes

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22
Q

phagocytes passed throughout

A

life

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23
Q

phagocytes function

A
  • Patrol in blood, tissues and organs
  • Remove dead cells and pathogens
    →By phagocytosis
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24
Q

phagocytes involved in

A

non-specific defense
→responds to many different non-self antigens

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25
Q

phagocytes appearance

A

Lobed nuclei
* Granular cytoplasm – due to many vesicles

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26
Q

Neutrophils

A

Multi-lobed nucleus
* Have receptor proteins on its membrane
→ To identify pathogens as non-self
* When there is an infection, large numbers
are released from bone marrow
→ Accumulate at site of infection

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27
Q

neutrophils lifespan

A

Short-lived (few hours-days)
→Dies after digesting pathogens
→Dead neutrophils form pus

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28
Q

Monocyte → Macrophage

A

Lobed nucleus / kidney-bean shaped
* Larger than neutrophils
* Have receptor proteins on its membrane
→ To identify pathogens as non-self

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29
Q

Monocytes circulate in

A

blood
→Mature into macrophages when it leaves
blood and enter organs

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30
Q

monocyte lifespan

A

Long-lived cells

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31
Q

Macrophages found in

A

organs such as
liver, lungs, spleen, kidney, lymph nodes

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32
Q

Role of Macrophages

A

Initiates / starts the immune response

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33
Q
A
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34
Q

macrophages mechanism

A

1) Has various receptor proteins of cell surface
* Can detect non-self antigens
* Non-specific
2) Engulf pathogen / foreign material via
phagocytosis (Chap 4)
* Fusion of phagocytic vacuole with lysosome
3+4) Cuts up pathogens using lysozymes
5) Antigens presented on its cell surface
→Macrophages act as
antigen-presenting cells (APC)
6) Some cell fragments released by exocytosis
* APCs can activate/stimulate lymphocytes

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35
Q

other APCs can include

A

B cells and other types of
phagocytes too!

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36
Q

Lymphocytes produced in

A

bone marrow before birth

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37
Q

lymphocytes function

A
  • Involved in specific immune responses
    →responds to only specific non-self antigens
  • Mature lymphocytes circulate in the blood
    and lymph
    →Accumulate at sites of infection
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38
Q

Appearance of lymphocytes

A

Smaller than phagocytes
* Large round nucleus
* Little cytoplasm

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39
Q

2 main types of lymphocytes

A

Both made in bone marrow, but mature in different places and
have different functions
1. B-lymphocytes (B cells)
* Mature in bone marrow
* Produces antibodies
2. T-lymphocytes (T cells)
* Mature in thymus
* Does NOT produce antibodies

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40
Q

both B cells and T cells

A

work together to defend the immune system

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41
Q

Millions of different types of B and T-lymphocytes with

A

receptors of different shapes

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42
Q

lymphocytes are

A

SPECIFIC = each type of lymphocyte responds to 1 type of
antigen only
E.g. Each type of B cell produce 1 type of antibody receptor
→which responds to 1 type of antigen only

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43
Q
A

So the body can respond to almost any type of pathogen

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44
Q

LymphocytesOnly mature lymphocytes

A

can circulate in the blood & lymph and
carry out immune responses

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45
Q

lymphocytes have

A

telomerase to divide continuously

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46
Q

Maturation of B-Lymphocytes

A
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47
Q

Maturation of B-Lymphocytes

A

1) All B cells are formed in the bone marrow before birth
→ Genes in B cells that code for antibodies code for diff types of
antibodies for diff types of B cells
2) Forms a specific antibody that acts as glycoprotein receptor on
surface membrane of B cells
→Binds to specific antigen that is complementary in shape
3) B lymphocytes divides and mature in bone marrow
→ Mature B lymphocytes circulate in blood and concentrate in liver,
spleen & lymph nodes

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48
Q

Antibodies
* Aka

A

immunoglobulins

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49
Q

antibodies are

A

Globular glycoproteins

50
Q

antibodies are made up of

A

4 polypeptide chains:
* 2 heavy chains
* 2 light chains

50
Q

antibodies have

A

Quaternary structure
Held together by disulfide bonds
→ gives stability

51
Q
A
52
Q

antibodies have 3 regions

A

1) Variable region (Fab)
2) Constant region (Fc)
3) Hinge region

53
Q

) Variable region (Fab)

A
  • Every chain has a variable region = 4 in total
  • Provide 2 identical antigen-binding sites
  • Specific for binding antigen
    → Complementary shape to antigen
    → Shape determined by primary structure
    = specific seq of amino acids
  • R groups at antigen-binding site forms H
    bonds and ionic bonds with specific antigen
    Sequence of amino acids at the variable region is
    different for each type of antibod
54
Q

Each type of antibody binds

A

different antigens

55
Q
A
56
Q

Constant region (Fc)

A
  • Formed by light and heavy chains
  • When circulating in blood: binds to receptors on phagocytes
  • When antibody acts as B cell receptor:
    attach to cell surface membrane of B cell
  • Gives antibody class
57
Q

3) Hinge region

A
  • Held by disulfide bridges
  • Gives flexibility when binding to antigen
58
Q

Action of Antibodies

A

Prevent entry into cell
Attach to flagella
Agglutination
Lysis of pathogen
Opsonisation
Neutralise toxins

59
Q
A

Prevent entry into cell

60
Q
A

Attach to flagella

61
Q
A

Agglutination

62
Q
A

Lysis of pathogen

63
Q
A

Opsonisation

64
Q
A

Neutralise toxins

65
Q

Action of B-Lymphocytes

A
  1. Pathogens invade
  2. Antigen presentation cell formation
  3. Only specific B lymphocytes has receptors with the
    complementary shape to antigen will be activated
    → Clonal selection
  4. B cell divides by mitosis
    → Clonal expansion
  5. Activated B cells develop into plasma cells and memory cells
66
Q

Plasma Cells

A
  • Short lived (few weeks)
  • Do not divide and do not have telomerase
  • Produce and secrete antibodies rapidly
    → by exocytosis
    → into blood plasma, lymph, lungs and stomach lining
  • Antibodies are glycoproteins
    → So plasma cells have extensive network of RER
    and Golgi
67
Q

Memory Cells

A
  • Long-lived, remain in circulation
  • Has telomerase
  • Provides long term immunity
  • Last for many years/lifetime
68
Q

memory cells during second invasion of same pathogen

A
  • Enable faster response during
    2
    nd invasion of same antigen,
    as many memory cells are circulating
  • During 2nd invasion, it divides rapidly (clonal expansion)
    →Form more plasma cells → more antibodies
    →Infection is destroyed before symptoms develop
    → Body immune to pathogen
69
Q
A
70
Q

Memory cells during Secondary response

A
  • Faster response
  • Many memory cells circulating
  • More cells specific for pathogen, higher
    chance of encountering pathogens quickly
  • More plasma cells formed
  • More antibodies produced
  • No symptoms developed
71
Q

Memory cells during primary response

A
  • Slower response
  • Only a few B cells specific
    to the antigen is present
  • Individual becomes ill
72
Q
A
73
Q
A
74
Q

Maturation of T-Lymphocy

A

1) All T cells produced in bone marrow before birth
2) Maturation in thymus gland
→ thymus shrinks after puberty
* Produce specific T cell receptors on cell
surface membrane
→Binds to specific antigen that is complementary in shape
→T cell receptor’s structure similar to antibodies
3) Mature T cells circulate in blood and lymph

75
Q
A
76
Q

Action of T-Lymphocytes

A
  1. Pathogens invade
  2. Antigen presentation cell formation
  3. Only specific T lymphocytes has
    receptors with the complementary shape
    to antigen will be activated
    → Clonal selection
  4. T cell divides by mitosis
    → Clonal expansion
  5. Activated T cells develop into
    T helper cells and T killer cells
77
Q

T helper cells function

A

1) Secrete cytokines / interleukins which
a) Stimulate specific B cells
* To divide and develop into plasma cells & memory B cells
* Increased antibody levels
b) Stimulate macrophages
* To carry out phagocytosis more
vigorously
c) Stimulate killer T cells
* To divide and produce more toxins

78
Q

T Helper Cells Functions

A

Form T helper memory cells
* Secondary response
* Long term immunity

79
Q

Cytotoxic T Killer Cells

A

1) Seeks out infected host cells (including APC, cancer cells)
and pathogens and destroys them
a) Attach to surface of cells
b) ‘Punch’ holes into cells
c) Secrete toxins into cells
* E.g. hydrogen peroxide,
perforin

80
Q

Cytotoxic T Killer Cells
Functions:

A

Forms killer T memory cells
* Secondary responses
* Long term immunity as it is long-lived

81
Q

2 types of immunity

A

active and passive

82
Q

active immunity

A

Own immune response is activated
– Own lymphocytes are activated by antigens
– Own antibodies are made
– Takes time, not immediate
– Memory cells formed → results in long-term immunity

83
Q

passive immunity

A

Immune response is NOT activated
– Own lymphocytes cells not activated
– NO plasma cells to produce antibodies
– Protection is immediate
– NO memory cells formed → only short-term immunity

84
Q
A
85
Q

Active Natural
Immunity

A

E.g. Catching a cold
Natural: Antigens
from the
environment

86
Q

Active Artificial
Immunity

A

E.g. Vaccination
Artificial: Antigens are introduced via injection into vein or muscle / consumed
→ activate the immune response artificially
Antigens can be attenuated / made harmless (e.g. heat-treated, cut up,
inactivated toxins)
Antigen used could be dead or alive

87
Q

Passive Natural
Immunity

A

E.g. Maternal antibodies
Natural:
1) Antibodies pass from mother infant through placenta
→ remain for months
2) Breast milk that is colostrum-rich has antibody (IgA) that prevents growth of bacteria/viruses in the stomach of infant

88
Q

Passive Artificial
Immunity

A

E.g. Antibodies or antitoxins
Artificial: Antigens are introduced via injection
Antibodies are collected from blood of donor / animals who are vaccinated or suffer from the same disease
→ Contains the specific antibodies against the specific antigen

89
Q
A
90
Q

Vaccination

A

activates the immune system
→ producing memory cells that result in
long term immunity

91
Q
A
92
Q
A
93
Q
A
94
Q

Effective Vaccines

A

Provide sufficient antigens
→ To mimic or copy natural infections
→ To form sufficient plasma and memory cells for long-term protection Give lifetime protection against pathogen
→ Pathogen unable to developed in immunised person
E.g. vaccines using live pathogens, smallpox vaccine

95
Q

Ineffective Vaccines

A

Do not mimic natural infections
→ No plasma and memory cells formed Do not give lifetime protection
→ Require booster injections
→ To stimulate secondary response in order to give protection Do not provide sufficient protection against pathogen
→ Maybe due to pathogen’s high mutation rate or ability to hide from immune system
E.g. vaccines using dead pathogens, cholera vaccine

96
Q

2 modes of vaccination

A

mass vacination
ring vaccination

97
Q

mass vacination

A

Vaccinate a large number of people at the same time

98
Q

Ring vaccination

A
  • Perform contact tracing with infected person
  • Vaccinate the area of community the person is in / people who was in contact with the person
99
Q

ring vaccination aim

A

Vaccinate a high proportion of the population
→ To achieve herd immunity

100
Q

Mass vaccination results in

A

herd immunity

101
Q

herd immunity advantages

A
  • Less chance of transmission of disease
    →Reduce pool of infected people in the community
    →Fewer people can catch the disease and be source of infection
  • Protection of those unvaccinated / immunocompromised as disease does not spread
102
Q

Common Barriers to Vaccinatio

A

1) Poor response to vaccines
* People that are immunocompromised
* People who lack protein (malnutrition)
* Less antibodies made
2) Pathogens can mutate rapidly (antigenic variation)
* Form diff strain with diff antigens
* Memory cells are unable to recognise pathogen that has major
changes in antigen structure
3) Pathogens can escape from immune system (antigenic concealment)
* By living inside cells / covering bodies with host proteins /
suppressing immune system

103
Q

How was smallpox eradicted?

A

An effective vaccine was developed!
* Same vaccine used everywhere
→ Variola virus – stable, low mutation rate
* Use live virus so strong immune response
→ similar Vaccinia virus
* One dose enough to give life-long immunity,
no boosters needed
* Vaccine is heat stable
* Easy to administer
→ Use bifurcated needle
→ Needle can be sterilized and reused

104
Q

Mass vaccination for smallpox was very successful!
This is due to:

A
  • High percentage of population immunized
    → Low cost needed to for mass production
    of vaccine
    → Many volunteers became vaccinators
    → Result in herd immunity
  • Infected people were easy to identify
    → Few symptomless carriers
    → Can perform contact tracing and
    ring vaccination
    → Can isolate cases to prevent spread
105
Q

Why isn’t TB eradicated already?

A

BCG vaccine is available!
* It is not eradicated even though there is a high coverage of
vaccination!

106
Q

why is TB not eradicated even though there is high coverage of vaccine

A
  • Vaccination does not work in adults >35yo
  • High percentage cover (above 90%) needed to achieve herd
    immunity
    → Not yet done in every country
  • Difficult for surveillance / to ensure vaccination
    → Due to high birth rates and high migration rates
    → Latent TB is symptomless and found in 1 in 4 people
107
Q

Why can’t we vaccinate against malaria?

A

No effective vaccines against malaria

108
Q

why is there no effective vaccine against malaria

A

Protoctists are eukaryotes
→ Many more genes than bacteria & viruses
* Display diff antigens on its cell surface for:
→ Diff species / strains
→ Different stages of its life cycle
* Parasite changes antigens during infection
→ Diff genes coding for antigens switch on during infection
* Plasmodium parasite hides in liver and RBCs

109
Q

Why can’t we vaccinate against cholera?

A

No effective vaccines against cholera
* Oral vaccination only gave limited protection as it was excreted

110
Q

why is there no effective vaccine against cholera

A
  • Many different strains of cholera
    → Bacterium mutates
  • Vibrio cholerae lives in the host’s intestines
    → Beyond reach of antibodies
111
Q

Monoclonal =

A

only 1 type of antibody, specific for 1 antigen

112
Q

problem with monoclonal antibodies

A
  • B cells that divide by mitosis DO NOT produce antibodies
  • Plasma cells that secrete antibodies DO NOT divide
113
Q

solution for monoclonal antibodies

A

Fuse plasma cells + cancer/myeloma cells
→ hybridoma cells that CAN divide and CAN produce antibodies

114
Q

how to produce monoclonal antibdoies

A

1) Inject foreign antigen (e.g. pathogen) into mice
2)Allow time for immune response tooccur
3) Collect plasma cells from spleen
3) Fuse plasma cells with cancer cells to produce hybridoma cells
→ Use fusogen for fusion
4) Clone hybridoma cells
→ Use HAT medium for hybridoma growth
5) Screen for cell secreting desired antibody
→ By separating cells and culture in individual wells
→ Select only one type
6) Grow hybridoma cells in large scale culture

115
Q
A
116
Q

diagnosis of using monoclonal antibodies

A
  • Monoclonal antibodies have same specificity and detects only
    one antigen
    → Can distinguish between diff pathogens / strains
    → Fast diagnosis than having to culture pathogen
    →Less labour intensive
    →Quicker diagnosis = quicker treatment
  • Can be tagged with a fluorescent label/dye
    →Can detect location of tissues expressing antigen
    →E.g. cancer cells, blood clots
  • Cheap, safe, fast results, easy to use, accurate
    (Also used in blood typing, pregnancy tests etc.)
117
Q

treatment using monoclonal antibodies

A
  • Used to target specific diseased cell by binding to receptors on
    its cell surface
    → Can kill cell by stimulating the immune system
    → Can attach radioactive substance / drug to Mabs to kill cell
  • Can bind to antigens on pathogens
    → Result in artificial passive immunity
118
Q

problems of using monoclonal antbodies in treatment

A
  • Causes some side effects
  • Antibodies made in animals recognised as non-self
  • Trigger immune response in humans
    → Allergic reaction
  • Remains in the body for short period of time as it is destroyed
  • Need to be administered more than once in small amounts
119
Q

solutions for the problems in using monoclonal antibodies in treatment

A

Humanise Mabs
1) Alter genes that code for heavy and light chains of antibodies
→ Code for human antibodies instead of mice and rabbit’s
2) Changing type and position of sugar groups attached to heavy chains
→ Arrangement of sugar groups same as human antibodies

9700 (14 decks)

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