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AS Biology > Chapter 11: Immunity > Flashcards

Chapter 11: Immunity Flashcards

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1
Q

what is immunity

A

ability to defend ourselves agaisnt infection by pathogens

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2
Q

2 types of defence mechanisms and their sub types

A
  • external: physical, chemical, cellular

- internal: white blood cells

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3
Q

describe the physical barriers function in defence against pathogens

A
  • skin doesnt let infectious agents penetrate unless broken
  • cilia and Mucus in the respiratory tract trap infectious agents
  • Acidic pH of the vagina – genito – urinary tract prevents entry of pathogen
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4
Q

describe the chemical barriers function in defence against pathogens

A
  • Acid in the stomach and enzyme in the intestine destroy pathogens.
  • Lysozyme in the tears, sweat and saliva avoids entry of the pathogens.
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5
Q

describe the cellular barriers function in defence against pathogens

A

Interferon mediated defence against viral infections. Interferons are cytokines that are secreted by virus infected cells which protect non infected cells from further viral infection.

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6
Q

where do wbc originate from

A

bone marrow

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7
Q

how do wbc recognise pathogens

A

by the distinctive, large molecules that cover their surfaces, such as proteins, glycoproteins, lipids and polysaccharides, and the waste materials which some pathogens produce.

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8
Q

molecules recognised as forgein are called

A

antigens

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9
Q

what makes the immune system effective

A

can distinguish between self and non self and has effective methods to fight eg antibodies

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10
Q

what are antibodies

A

glycoprotein/immunoglobulin molecules that act against specific antigens.

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11
Q

what is an antigen/non self

A

a substance that is foreign to the body and stimulates an immune response.

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12
Q

Antibodies are made by _ and made when _.

What about the variable region of it?

A

plasma cells derived from B-lymphocytes, secreted in response to an antigen; the variable region of the antibody molecule is complementary in shape to its specific antigen.

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13
Q

what is the immune response

A

the complex series of responses of the body to the entry of a foreign antigen; it involves the activity of lymphocytes and phagocytes

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14
Q

what does self refer to

A

substances produced by the body that the immune system does not recognise as foreign, so they do not stimulate an immune response.

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15
Q

2 groups of wbc involved namely…

A
  • phagocytes (neutrophils and macrophages)

- lymphocytes (b cells and t cells)

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16
Q

where are phagocytes made and what is their function

A
  • made throughout life in bone marrow

- remove dead cells and invasive organismss

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17
Q

what are neutrophils

A
  • kind of phagocyte
  • 60% of wbc
  • travel body, by squeezing through capillary walls to patrol tissues
  • short lived. collect at site after death forming pus
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18
Q

what are macrophages

A
  • phagocytes, larger than neutrophils
  • found in organs such as the lungs, liver, spleen, kidney and lymph nodes rather than in blood
  • travel in blood as monocytes after made in bone marrow
  • long lived
  • do not destroy pathogens but cut em up into antigens for lymphocytes to recognise
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19
Q

describe the process of phagocytosis

A
  • cells under attack during an infection produce histamine, which along with other pathogenic chemicals attract neutrophils
  • pathogen may be a cluster and covered in antibodies which the neutrophils protein receptors on surface attach to
  • so neutrophil attaches to pathogen and engulfs it with membrane via endocytosis and traps it in a phagocytic vacuole and secretes digestive enzymes eg protease into it (lysosome fusion)
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20
Q

what is chemotaxis

A

movement towards chemical stimuli

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21
Q

structure of lypmhocytes

A
  • smaller than phagocytes

- large, filling nucleus

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22
Q

2 types of lymphocytes and their production+maturation

A
  • B cells: remain in the bone marrow until they are mature and then spread throughout the body, concentrating in lymph nodes and the spleen
  • T cells: leave the bone marrow and collect in the thymus where they mature (the thymus is a gland that lies in the chest just beneath the sternum. It doubles in size between birth and puberty, but after puberty it shrinks)
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23
Q

vividly describe the mechanism of B-lymphocyte action

A

-as B cell matures its able to make 1 type of antibody receptor with specific shape. while B cells mature genes that code for antibodies are changed in a variety of ways to code for different antibodies.
-each cell then divides to a small group of cells called clones which can make that 1 antibody and conc in liver+spleen
-antibodies remain on cell membrane acting as glycoprotein receptors specific to an antigen
-when anitgen enters the small no. of cells with the antibody stimulated to divide by clonal selection and produce many identical cells over few weeks in clonal expansion
-some activated B cells become plasma cells and secret antibodies at a high rate into blood,lymph nodes, lung and gut linings
-others form memory cells which ciruclate in blood for long
-If same antigen is reintroduced
memory cells divide rapidly and develop into plasma cells and more memory cells

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24
Q

life span of plasma cells, memory cells and antibodies

A

memory>antibody>plasma

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25
Q

Changes in the concentration of antibody molecules in the blood when the body encounters an antigen first and later

A

Primary response: slow, few antigen specific B cells antibodies
Secondary response: faster, many memory cells which can differentiate into plasma cells–>antibodies

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26
Q

memory cells are the basis of

A

immunological memory

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27
Q

Application of primary and secondary responses

A
  1. someones unlikely to get measles twice because only one strain of virus so very fast 2ndry response
  2. we suffer repeated infections of the common cold and influenza because there are new and different strains of these viruses each with diff antigens
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28
Q

antibody structure

A
  • globular protein with quarternery structure
  • 4 polypeptide chains (constant region): 2 heavy/long 2 light/short. disulfide bonds hold chains together
  • each has 2 identical antigen binding sites made of BOTH heavy+light chains
  • sequences of amino acids in these regions make the specific 3D shape which binds to 1 type of antigen
  • ‘hinge’ region gives the flexibility for the antibody molecule to bind around the antigen.
  • have chain sugars attached
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29
Q

what is diff in each type of antibody

A

antigen-binding sites form the variable region

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30
Q

6 antibody action mechanisms

A

1) combine with virus/bacterial toxin preventing cell entry+damage
2) attach to flagella of bact and make em less active and easier for phags to engulf
3) antibodies with multiple binding sites cause agglutination/clumping and reduce spread
4) along with other molecules they puncture holes in cell wall which leads to burtsing after osmosis
5) markers ie coat bact, phags have receptors for heavy polypeps
6) antitoxins combines with toxins and neutralise em making them harmless

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31
Q

types of antibodies named

A

Ig A,D,E,G,M

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32
Q

iga structure+property

A

dimer

Found in mucus, saliva, tears and breast milk. Protects against pathogens

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33
Q

igd structure+property

A

monomer

Part of the B cell receptor. Activates basophils and mast cells

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34
Q

ige structure+property

A

monomer

Protects against parasitic worms. Responsible for allergic reactions

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35
Q

igg structure+property

A

monomer

Secreted by plasma cells. Also cross placenta to enter fetus

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36
Q

igm structure+property

A

pentamer

May be attached to the surface of B cell or secreted into the blood. Responsible for early stages of immunity.

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37
Q

features of neutrophils

A

Multilobed, Bacterial or fungal infection. These are the common first response to microbial infection

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38
Q

features of eosinophils

A

Bilobed, Parasitic infections and allergic reactions (inflammatory)

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39
Q

features of basophils

A

Bi/ Trilobed, Allergic and antigen response (releases histamine causing vasodilation)

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40
Q

features of lymphocytes

A

Include B lymphocytes and T lymphocytes. Large circular nucleus with little cytoplasm

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41
Q

features of monocytes

A

Kidney shaped nucleus, Phagocytosis of pathogens. Presentation of antigens to T lymphocytes. Eventually they become tissue macrophages which remove dead cells and attack microorganisms.

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42
Q

mechanism of T-lymphocyte action

A
  • mature T cells have specific cell surface receptors called T cell receptors, structure similar to that of antibodies, and they are each specific to one antigen.
  • activated when they encounter this antigen (complementary to receptor) on another cell of the host eg macrophage upon antigen representation
  • clonal selection and expansion
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43
Q

3 types of T cells

A

a) helper T cells
b) killer T cells (or cytotoxic T cells)
c) suppressor T cells

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44
Q

what happens when helper t cells are activated

A

they release hormone like cytokines that stimulate appropriate B cells to divide, develop into plasma cells and secrete antibodies.
some T helper cells secrete cytokines that stimulate macrophages to carry out phagocytosis more vigorously.

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45
Q

what happens when killer t cells are activated

A

search body for cells that have become invaded + are displaying foreign pathogen antigens on their cell membranes
they recognise the antigens, attach themselves to the surface of infected cells, secrete toxic substances eg H2O2, killing the body cells and the pathogens inside.

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46
Q

what happens when suppresor t cells are activated

A

suppress immune response of the body by suppressing the action of B and T lymphocytes.

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47
Q

memory t cells

A

remember antigen for future

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48
Q

what are platelets

A

small cell fragments that do not have a nucleus; they are formed from the break-up of cells in the bone marrow.
release substances that stimulate blood clotting

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49
Q

how are results for specific white blood cells given

A

as absolute numbers or as percentages of the white cell count

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50
Q

when does neutrophil count increase

A

during bacterial infections and whenever tissues become inflamed and die.

51
Q

when does lymphocyte count increase

A

viral infections and in TB

52
Q

which cells does HIV invade and destroy

A

helper T cells

53
Q

state the cycle of from bone marrow to individual wbc types

A

bone marrow stem cells–>hematopoietic cell–>Lymphoid progenitor makes B and T cells OR–>Myeloid progenitor which make platelets,eosiniphil,basophil,neutrophil,monocyte,erythrocyte

54
Q

what happens in leukemia

A

it is the cancer of stem cells that divide to give rise to huge nos of mature differentiated blood cells which function in specific parts of immune response

  • so when they divide uncontrollably they dont properly differentiate and disrupt function of normal rbc and platelets
  • These malignant cells fill up the bone marrow and then flow into the blood and into the lymphatic system
55
Q

what is myeloid leukemia

A

stem cells responsible for producing neutrophils divide uncontrollably and the number of immature cells increases

56
Q

what is lymphoblastic leukemia

A

the cancerous cells are those that give rise to lymphocytes

57
Q

long term affect of leukemia:

A
  • immature wbc produced very quickly and disrupt normal balance of components in blood. body does not have enough rbc or platelets, causes anaemia and increases risk of excessive bleeding.
  • numbers of mature neutrophils and lymphocytes decrease so that people with these cancers become more susceptible to infections ie immunosuppressed
58
Q

acute and chronic leukemia

A
  • acute develop quickly, have severe effects, and require immediate treatment upon diagnosis
  • chronic take years to developand changes in blood cell counts are usually monitored over time so that treatment is given when it is most likely to cure the disease
59
Q

how can leukemia be diagnosed, monitor their progress and assess treatment effectiveness

A

blood tests

60
Q

what is active immunity

A

immunity gained when an antigen enters the body, an immune response occurs and antibodies are produced by plasma cells

61
Q

what is a downside of active immunity

A

It takes time for sufficient numbers of B and T cells to be produced to give an effective defence

62
Q

what is natural active immunity

A

lymphocytes are activated by antigens on the surface of pathogens that have invaded the body during an infection

63
Q

what is artificial active immunity

A

lymphocytes activated by injecting antigens into the body or –for certain diseases– taking them by mouth.
aka vaccination

64
Q

define vaccination

A

giving a vaccine containing antigens for a disease, either by injection or by mouth; vaccination confers artificial active immunity

65
Q

what is passive immunity

A

immunity gained without an immune response; antibodies are injected (artificial) or pass from mother to child across the placenta or in breast milk (natural). antibodies not produced by person as B cells not activated

66
Q

advantages of artificial passive immunity

A

If a person becomes infected with fatal disease such as tetanus, a more immediate defence than active immunity is needed for survival. Tetanus kills quickly, before the body’s natural primary response can take place. So people who have a wound that may be infected with the bacterium that causes tetanus are given an injection of antitoxin. This is a preparation of human antibodies against the tetanus toxin.

67
Q

disadvantages of artificial passive immunity

A

Antitoxin provides immediate protection, but this is only temporary as the antibodies are not produced by the body’s own B cells and are therefore regarded as foreign themselves. They are removed from the circulation by phagocytes in the liver and spleen.

68
Q

define natural immunity in terms of active and passive

A

gained by being infected (active) or by receiving antibodies from the mother across the placenta or in breast milk (passive).

69
Q

how newborns aquiring antibodies and the protection they gain from this…

A

Infants are not entirely unprotected against pathogens, because antibodies from their mothers cross the placenta during pregnancy and remain in the infant. Colostrum, the thick yellowish fluid produced by a mother’s breasts for the first four or five days after birth,contains a type of antibody known as IgA. Some of these antibodies remain on the surface of the infant’s gut wall, while others pass into the blood undigested. IgA acts in the gut to prevent the growth of bacteria and viruses and also circulates in the blood.

70
Q

summarise active, passive and subtypes natural, artificial

A

A-pathogen in body. N-infection A-injection of live/attenuated pathogen
P-antibodies/antitoxins from outside body. N-from mother A-injection

71
Q

features of active and passive immunity ie antigen encountered, immune response, time before anitbodies in blood, memory cells, protection duration

A 
A-antigen. P-no
A-response. P-no
A-1/2weeks. P-immediate
A-memory cells. P-no
A-permanent protection. P-temporary
72
Q

conc of antibodies in mother and a fetus before and an infant after conception to within a year (that graph)

A
  • till birth maternal and fetus antibodies rise. fetus gains natural immunity IgG via placenta
  • after birth maternal decreases and infants increases due to milk/colostrum IgA
73
Q

what are live attenuated vaccines

A

contain the microorganism/pathogen but a weakened lab version. it evokes the immune system of host hence prevents actual disease in the future

74
Q

eg of vaccines that use live attenuated method

A

measles, chicken pox, yellow fever, typhoid

75
Q

live attenuated vaccines are easy to create for certain viruses but not for bacteria. why is this

A

bacteria have thousands of genes and are harder to control

76
Q

live attenuated vaccine mechanism in more detail at cellular level

A
  • whole organism is used as vaccine but its effect reduced almost or fully as of being devoid of pathogenicity
  • but capable of inducing protective immune response
  • multiply in host and provide continuous antigenic stimulation over a period of time
77
Q

what are inactivated vaccines

A
78
Q

advantages of inactivated vaccines over live ones

A
  • safer and more stable; d microorganismscan’t mutate back to their disease-causing state
  • easy preparation to use
  • usually don’t require refrigeration, and can be stored and transported in a freeze-dried form, which makes them accessible in developing countries.
79
Q

disadvantage of inactivated vaccine over live

A

Less effective;

-dead microorganisms do not multiply in body as to mimic the infection

80
Q

eg of chemicals used to kill pathogens for vaccines

A

-formaldehyde or beta-propiolactone

-

81
Q

what is the traditional agent for inactivation of virus

A

formalin

82
Q

the specifically tricky thing with treating organisms in inactivated vaccines

A

Excessive treatment can destroy immunogenicity (ability of a foreign antigen to provoke response) whereas insufficient treatment canleave infectious microorganisms capable of causing disease.

83
Q

eg of inactivated vaccines

A

cholera, plague, influenza, rabies, rubella, hepatisis A

84
Q

what are subunit vaccines

A

Vaccine that consists of specific, purified macromolecules derived from pathogen:
-instead of the whole microorganism only the antigens which best stimulate immune response used to prepare vaccine

85
Q

3 general forms of subunit vaccines

A

Purified capsular polysaccharides, inactivated exotoxin (toxoid), recombinant microbial antigen

86
Q

what is a conjugate vaccine

A

Is a substance that is composed of a polysaccharide antigen fused (conjugated) to a carrier molecule eg an antigen which infants system knows. This enhances the stability and the effectiveness of the vaccine.

87
Q

what are toxoid vaccines

A
  • for bacteria that secrete toxins/harmful chemicals

- toxin inactivated with formalin to detoxify it resulting in toxoid used as vaccine

88
Q

how do toxoids work

A

induce anti toxoid antibodies which learn how to bind to natural toxin and neutralize it

89
Q

eg of toxoid vaccines

A

tetanus and diphtheria

90
Q

conditions for toxoid vaccine production

A

must be closely controlled to achieve detoxification without excessive modification of the epitope structure. Sufficient quantities of the purified toxins is prepared by cloning the exotoxin genes and thenexpressing them in easily grown host cells, purified and subsequently inactivated

91
Q

what are recombinant vector vaccines

A

They’re experimental vaccines similar to DNA vaccines, but they use an attenuated virus or bacterium to introduce microbial DNA to cells of the body.

92
Q

how do recombinant vector vaccines work

A
  • The gene coding for immunogenic protein is inserted into plasmid vector and thentransformed it into suitable host cell
  • The inserted genetic material causes the cell to display the antigens of the microbe on its surface
  • In effect, the harmless cell mimic harmful microbe and stims a response
93
Q

eg of recombinant vector vaccines

A

Hepatitis B only

94
Q

why do less effective vaccines need boosters

A

to stimulate secondary responses that giveenhanced protection

95
Q

state 4 problems with vaccines

A
  • poor response
  • live virus and herd immunity
  • antigenic variation
  • antigenic concealment
96
Q

explain poor/zero response of some people to vaccines and their contribution to eradication

A
  • may have defective immune system so dont develop B and T clones
  • malnutrition especially protein deficiency doesnt allow making of anitbodies and lymphocyte clones

they are high risk of developing infectious diseases and transmitting them to those with no immunity

97
Q

explain problems with live virus, and herd immunity

A
  • People vaccinated with a live virus may pass it out in their faeces during the primary response and may infect others. This is why it is better to vaccinate a large number of people at the same time to give herd immunity, or to ensure that all children are vaccinated within a few months of birth
  • Herd immunity interrupts transmission in a population, so that those who aresusceptible never encounter the infectious agents concerned
98
Q

the issue with antigenic variation and vaccines:

A
  • viruses with many strains eg cold/rhinovrius

- antigen mutations eg influenza

99
Q

explain antigenic drift and shift

A

drift-minor changes which memory cells can still identify and start decondary response
shift-major structural changes where vaccine becomes ineffective against new one

100
Q

why have no effective vaccines been made against protoctist caused diseases

A

-eukaryotic pathogen so have more genes than virus/bacteria and even more surface antigens

101
Q

why is there no vaccine agaisnt malaria

A
  • parasite passes 3 stages in lifecycle in host, each with its own specific antigens
  • meaning vaccine has to have antigens to all 3… or specific to each, which can work only if immune system effectively responds to each within short time eg between bite and liver cell infection
102
Q

the issue with antigenic concealment and vaccines: (ways)

A
  • some pathogens live inside host cells to evade antibodies
  • some worms cover their bodies in host proteins
  • others suppress immune system by parasitising cells like Tcells and macrophages
  • V.cholerae stays in intestine far from antibodies

Hence short time for an immune response to occur before it hides so vaccines are hard to make

103
Q

what are autoimmune diseases

A
  • when the immune system attacks itself ie self antigens usually proteins
  • when t cells mature in thymus many are destroyed cos they have receptops complementary to self antigens so when they evade this and sometime activated to stimulate response to own proteins
  • antibodies and killer Tcells work against diff parts; localised organ/whole body
104
Q

elaborate on what happens in a pateints body when they develop myasthenia gravis

A
  • motor neurons transmit nerve impulses to muscle cells, by releasing acetylcholine-signalling molecule- into gap between neuron and fibre. Acetylcholine interaction with receptors proteins on muscle cell membrane stims channels to open and Na+ move through and this results in some events which result in contraction.
  • MG ppl have helper T cells specific to these receptors and under certain conditions stim a B cells clone to make plasma cells and antibodies to bind to receptor to block impulse transmission from neuron. Muscle fibres absorb receptor-antibody complex and destory it. without receptops muscles not stimmed so tissue breaks down
105
Q

what is myasthenia gravis

A

autoimmune disease that targets the neuromuscular junctions between motor neurons(nerve cells) and skeletal muscle cells.

106
Q

MG symptoms

A

varies between ppl

but typical muscle weakness and hence fatigue; worse with activity, improved with rest

107
Q

2 effective MG treatments

A
  • a drug that inhibits the enzyme in synapses which breaks down acetylcholine so as to increase its conc. n synapses so it lasts longer stimming
  • surgical removal or thymus gland (because its site of maturation of helper T cells that stimulate B cells to produce antibodies to the acetylcholine receptors)
108
Q

what is multiple sclerosis

A

develops when nerve cells in the brain and spinal cord (CNS) randomly lose the insulatingmyelin sheaths that surround them.

109
Q

degenerating areas in multiple sclerosis known as

A

plaques

110
Q

what progresses with the loss of the protective myelin in MS

A

The neurones stop conducting impulses and there is a loss of thefunctions controlled by the areas of the CNS concerned

111
Q

multiple sclerosis symptoms

A

muscle weakness, loss of sensory input from the skin and other areas, poor vision and mental problems

112
Q

no card

A

ok

113
Q

what is rheumatoid arthritis

A

long term destructive process in the joints are swollen and cant stretch
starts with finger and hand joints and spreads to shoulder etc
endons become inflamed and there is constant muscle spasm and pain. and ppl cant keep still

114
Q

reasons for autoimmune diseases

A

Genetic factors increase susceptibility to the diseases are inherited. However, environmental factors are also contribute as the increase in prevalence of these diseases in the developed world

115
Q

Antibodies have high degrees of specificity. This specificity of antibodies has made them very desirable for use in the treatment of diseases. Nevertheless, this requires a very large number of cells of a particular B cell clone, all secreting identical/ monoclonal antibodies (Mabs), but this isnt possible as…

This is tackled by scientists using the method of…

A

…cells that divide by mitosis do not produce antibodies, and plasma cells that make anitbodies dont divide

… small number of plasma cells producing a particular antibody are fused with cancer cells-which divide indefinitely- forming a hybridoma which divides by mitosis to form the Mabs

116
Q

Mabs in diagnosis of clots

A
  • locate blood clot position in deep vein thrombosis
  • human fibrin-main clot protein-injected in mouse, which makes plasma cells to make antibodies agaisnt foreign fibrin. these are collected from spleen, fused with cancer. hybridoma makes antifibrin antibody which is radioactively labelled with gamma producing chemical and then put in patients bloodstream where they bind to any fibrin and this can be detected by gamma ray camera
117
Q

Mabs in diagnosis of cancers

A

-cells have proteins in their cell surfacemembranes that differ from the protiens on normal body cells and can therefore be detected by antibodies

118
Q

how is the fact that Mabs can be used to identify the exact strain of a virus or bacterium (diff antigen on surface than normal body cells then same process) that is causing an infection helpful to doctors

A

speeds up the time to take an appropriate treatment decision by narrowing down the possible choices

119
Q

Mabs are also used routinely in blood group typing before transfusion, and tissue typing before transplants.

A

antigen on rbc different

120
Q

Mabs in diagnosis adminstered once. In treatment more than once and this is problematic bcos…
This issue has been overcome by….

A

antibodies are made by lab animals and trigger and immune response because they are foreign

  • altering the genes that code for the heavy and light polypeptide chains of the antibodies so that they code for human sequences of amino acids, rather than mice sequence
  • changing the type and position of the sugar groups that are attached to the heavy chainsto the arrangement found in human antibodies
121
Q

trastuzumab: to treat what+how

A
  • treating breast cancers
  • binds to hercepin receptor protein (not unique to cancers but when in abnormal quantities its confirmed cancer)
  • marked for destruction
122
Q

ipilimumab: to treat what+how

A
  • melanoma a type of skin cancer
  • secretes antibody that binds to protein produced by T suppressor cells as to inhibit it
  • blocks its action and maintains immune system agaisnt cancer
123
Q

infliximab: treats what+how

A
  • rheumatoid arthritis
  • binds to protein secreted by Th and Tk that damage cartilage in joints
  • so sorta suppresses immune system
124
Q

rituximab: treat what+how

A
  • leukemia (also for those 3 autoimmune diseases). here theres over/inappropriate B cell production
  • controls B cells
  • this antibody binds to B cell receptors-antigens and leads to changes to kill the abnormally proliferated undifferentiated B cell

AS Biology (11 decks)

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