Summary
Summary CCEA GCE Biology - Chapter 2 - Immunity
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Immunity mindmap based on A2 1 CCEA chapter 2.
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I-
Herd immunity - a high enough proportion of Antibodies made in another individual, which
Transplanted organs contain non-self antigens are harvested and injected into another person
Primary response Secondary response the population is vaccinated and those who
↑F
- -
RBC's have antigens on their cell surface, if they come from somewhere else. Transplants = Time as a serum. They can be taken from individuals
·
-
fail as they get rejected. T-lymphocytes are -
are not vaccinated are less likely to catch a
the ABO system which is an example of Initial delay - -
particularly infectious disease. Very recovering from illnesses. Previously, using
Antibody conc.
polymorphism» a situation where there sensitised by non-self antigens present in followed by -
Antibody levels remain high
animals ( eg. horses) and immunising them with
-
transplanted tissue, which are cloned by relatively slow - -
for a much longer period of important in protecting those who can't get
are several distinct categories or forms. mitosis to produce killer T cells and they
increase in time than in the primary
vaccinated eg. Newborns and the ill. attenuated pathogens or their inactivated
=
-
antibody
Group O is considered the universal donor destroy the transplanted cells. To avoid production
Vaccination programmes are expensive but toxins, then creating a serum (Blood plasma • The phagocyte moves towards the
and AB lacks both anti-a and anti-b rejection: tissue typing- matches the donor and Rapid increase in economic benefits are: with clotting substances removed) from the pathogen, attracted by the chemicals it
antibodies and is the universal recipient. recipient cell surface markers (antigens) so antibodies produced and it is given to individuals
=
antibody conc. to a
much higher - lower treatment costs to treat ill people. produces.
When transfused info a wrong type an that there is the best match possible. The best - employees do not take as much time off work requiring rapid immunity. Most common is
maximum • As it does so the phagocyte membrane
antigen-antibody reaction occurs causing tissue matching will take place bet ween close therefore productivity increases. monoclonal antibody production which removes
relatives. Immunosurpression techniques - such Initial exposure invaginates to begin to close the pathogen.
agglutination. The rhesus system is based Second exposure
- carers don't have to take time off work to sensitised and cloned b-lymphocytes from a
as drugs to inhibit DNA replication and to antigen to antigen • As the pathogen is engulfed, the
on the presence or absence of the rhesus look after the sick. Antibodies passing mouse that has been infected with a particular
therefore cloning of lymphocytes will how unvaccinated phagocyte membrane forms
antigen. Rhesus positive = having the from mother to baby antigen. The mouse b-lymphocytes are
down or stop the rejection. X-rays - used to a phagosome (vesicle) around the pathogen.
rhesus antigen whereas rhesus negative across the placenta
I
inhibit the production of lymphocytes through Vaccinations produce a primary immune response after tricking the immune hybridised with cancer cells to produce lag • Lysosomes move towards the phagosome
individuals don't have the antigen. Anti-d or in the colostrum, living lymphocytes that can produce the
irradiation of bone marrow or lymph tissue. system into thinking the body has been infected therefore the body is and fuse with it.
antibodies do not occur naturally in the Unpleasant side effects can result and so it is it is crucial in early required antibodies continuously over a long
equipped to produce a secondary response. Vaccinations usually contain: • Hydrolytic enzymes within the lysosomes
plasma. An individual who is Chers positive used as a backup. Immunosurpression will life when the baby's period of time - advantages include: can be
• killed or weakened (attenuated) pathogens which contain the antigens are released into the plagosome, onto the
will not produce anti-d antibodies. Rhesus compromise the recipients immune system immune system is produced in large quantities in the lab, can
required to produce an immune response but will not cause the disease pathogen - the enzymes hydrolyse the
negative individuals don't have the which makes the individual susceptible to still developing produce a single type of antibody instead of
itself. pathogen.
antibodies, but is their blood becomes infection as it depresses the immune system in having unwanted chemicals that can
general. • modified toxins produced by the pathogen - with some pathogens it's the • The soluble digested products are absorbed
contaminated with blood containing potentially cause allergies.
toxins that produce the immune response, they must be modified and into the cytoplasm of the phagocyte.
antigen D from: A blood transfusion
made harmless but not changed too much that they don't produce an Natural
bet ween a rhesus positive donor and a
During birth/late pregnancy immune response. Phagocytes including polymorphs (the most common and first to arrive) and macrophages
negative recipient. Or when a rhesus Transplant
some foetal red blood cells • isolated antigens separated from the pathogen itself - for some the (develop from monocytes in the blood, they are larger but much longer pathogenic bacteria
negative mother has a rhesus negative (rh+ to contain antigen D) Blood transfusions tissue Artificial
antigens can be made by genetic engineering. and lived than polymorphs) are able to squeeze through the capillary walls and engulf the
baby. leak into the mother’s
circulation. pathogens and surrounding cell debris at the site of infection.
Antigens on RBC Antibodies in plasma Develops through having the disease in which the individual↑ Rapid immunity as
Causes rh- mother's immune
becomes ill but recovers due to a primary response. If infected sensitisation and plasma cell
A A Anti-b again by the same pathogen, the secondary response is rapid that production do not happen first. Rapid response by WBCs called phagocytes As part of an inflammatory response following
system to produce anti-d
antibodies. By the time the immune system may destroy the pathogen before feeling ill. It is helpful when someone infection the capillaries in the affected area
B B Anti-a Artificial Phagocytosis become leaky, allowing plasma to seep into the
antibodies are produced in The primary immune response is slow to develop and the gets infected with a pathogen
AB A+ B Neither Anti-a
Anti-b
significant numbers the baby is individual suffers the disease symptoms for a period of time but Natural they have no defense against into the surrounding areas. Inflamed parts of the
born - there is no threat to body tend to become swollen with phagocytes,
once in place it is long lasting. The very strong and rapid but it is only temporary HCI - in stomach, kills pathogens that are in foods/
O None Both Anti-a the baby.
dead pathogens and cell debris - pus. Inflamed
Anti-b secondary response is due to there being many more memory cells drinks. Provides a very low pH which denatures enzymes.
than specific b-lymphocytes at the start of the primary response Lysozyme (in saliva, tears and sweat) which hydrolyses areas appear red due to increased blood flow, and
Rhesus -ve mothers are treated at 30 In subsequent pregnancies, if the foetus Active hat as the raised temperature reduces infection
and the memory cells are already sensitised. Production of Passive bacteria cell walls. Tears can also wash away debris.
weeks by being given an injection of is rh+ the mother is already sensitised Antibodies from another source
by denaturing enzymes.
anti-d antibodies which attach to any and large numbers of anti-d antibodies antibodies by their Non specific
can be produced immediately if any Antibiotics: disrupt cell wall formation by inhibiting an own body Skin - tough physical barrier that most pathogens
antigen D containing foetal red blood cell foetal blood cells enter the maternal enzyme involved in the process. Bacteria are killed as the cannot penetrate unless there are wounds/cuts.
fragments that may pass across the circulation. The anti-d antibodies can
placenta and enter the mother's
cross the placenta and cause cell bursts, as it can't resist osmotic pressure due to a Immunity Lines of defence
Epithelial lining covered in mucus eg. in the respiratory tract, which traps
agglutination of foetal red blood cells, weakened cell wall. They can also inhibit metabolic
circulation before the mother's b- haemolytic disease of the newborn.
processes including protein synthesis, erythromycin pathogens which prevents them penetrating the underlying membranes.
lymphocytes are stimulated to produce destroys ribosomes in prokaryotic cells. Production of T cells stimulated by antigen Specific Cilia, tiny hairs lining the respiratory tract sweep mucus and it traps
anti-d antibodies. Following birth, is the presenting cells: pathogens back up the trachea.
baby is rh+ve another injection of anti-d • Macrophages (phagocytes) that have
antibodies is given within 72 hours. If Antibiotic resistance How rapidly a disease spreads: how engulfed and broken down a pathogen
Targets microorganisms - bacteria /viruses, found in the body fluids.
screening/testing is bypassed the baby easily it spreads, how likely someone and 'present' some of the pathogen's
Antibodies are globular proteins which are complementary to specific
can be treated by blood transfusion. will fall ill, whether there is a antigens on their own surface Self/non-self - non-self are not recognised by the body. If detected
antigens. Antigens sensitive specific b-lymphocytes that have receptors
vaccination. Viruses are more likely membrane. by their different antigens they produce an immune response.
that match the pathogens antigens and the b-lymphocyte becomes cloned.
to become an epidemic/pandemic due • Any type of cell invaded by a virus - There is a specific immune response based on the antigens, due to
Antibodies latch onto bacterial antigens dumping the bacteria together
Mutations in the bacterial genome lead to metabolic changes that result in to: small genomes that are prone to again some of the viral antigens are the lymphocyte having complementary receptors on the cell
the build up of antibodies enable a sufficient number to be present to
antibiotics no longer being effective. Bacteria reproduces rapidly by binary fission, mutation, retroviruses with RNA in presented on the cell surface membrane surface membrane. Lymphocytes that are complementary in shape
immobilise the bacteria causing agglutination or clumping as an antigen-
one resistant bacteria can lead to a large population of antibiotic resistant the genome which are less stable of the body cell. with foetal cells are 's witched off' so by the time the baby is born
antibody complex to then be engulfed by polymorphs and other phagocytes.
bacteria. Some antibiotic resistant bacteria are resistant to a number of than one with DNA, antibiotics • Cancer cells, as many types of cancer the functional lymphocytes are the ones that are complementary
Antibodies can also destroy invading cells directly or act as opsonins by
antibiotics and it is a risk that some strains could became resistant to all aren't effective against viruses. cells present abnormal antigens on their to non-self cells. The specific immune response is relatively slow -
attaching to pathogens and marking them for phagocytosis.
antibiotics. More vigorous hygiene culture in hospitals, more effective isolation of cell surface membranes. there are only a few of each type out of the million functional
Antigen-antibody complex
infected patients (eg. with MRSA), a more judicious approach to antibiotic use and lymphocytes. Antigens on pathogen immobilises pathogens (to be
destroyed by phagocytosis)
targeted new drug treatments. Same benefits as vaccines. Animals as reser voirs Antibody mediated immunity
Cell mediated immunity
T-lymphocytes B-lymphocytes -
Animal species that harbour viruses which subsequently cause disease in humans are described as reser voirs. Bats have • Formed in stem cells in the bone marrow • Formed in stem cells in the bone marrow.
been reservoirs for the viruses that cause Marburg, SARS, and Nipah. Bats are mammals with very similar physiology • Matures in bone marrow • Matures in the thymus gland.
to humans, they're social animals and are in very close contact with large numbers of other bats therefore a high Memory T cells • Antibody mediated response • Cell mediated immunity.
proportion of the species are carriers, increasing the possibility of cross infection. They fly large ranges and therefore • Produces antibodies which respond to antigens • Responds to antigens attached to body cells. Antibodies produced by
plasma cells are
are potentially in contact with other organisms. Circulate in body found in body fluids which respond to bacterial or Respond to body cells affected by viral infection. complementary in shape to
pathogen antigens
fluids and respond viral infection.
rapidly to Memory cells
Diagnosing infection reinfection by the Suppressor T cells Plasma cells
Killer T cells Helper T cells
ELISA techniques and detection of cytokines as biomarkers. Cytokines are molecules involved in signalling bet ween same pathogen Live for many years in body fluids and remain
different types of immune cells and increase cytokine concentration can represent an increased immune response and are memory cells ave Supress the immune Short lived - but produces many inactive unless stimulated by the presence of the
Cytotoxic T cells Stimulate other cells millions of antibodies, which are
used as biomarkers to identify conditions. Elisa (enzyme-linked immunosorbent assay) → a lab technique which uses already sensitised response of other immune destroy infected same antigen/pathogen again, which would cause
and very rapidly involved in the necessary to destroy the memory cells to divide rapidly and provide vast
antibodies, enzymes and other molecules as biomarker, to detect the presence of particular molecules in the body. ELISA cells when required. They cells by attaching to
produce a large immune response eg. pathogen while the memory numbers of plasma cells as there are mostly
assays can test for a small or large number of potential antigens or biomarkers at the same time, therefore screening for switch off an immune the antigens on the
clone of T They stimulate b-cells cells provide a guarantee of long memory cells in the secondary immune response.
a large number of possible conditions. Body fluids are added to a number of wells on a plate and a range of antibiotics are response after invading cell surface
lymphocytes. to divide and promote term protection.
added to these wells. Reaction bet ween antibody and antigen triggers an enzyme linked to the antibody into causing a microbes and infected membrane by the phagocytosis through
colour change, identifying antigens or other molecules present. ELISA diagnostic kits used to detect: pathogens in the cello have been infected or Phagocytosis is a slow process without the activating role of
their effect on
body, cancer cell markers, cardiac disease markers, pregnancy. They enable early, rapid screening and can provide a wide destroyed. They are also abnormal cell and Phagocytosis the helper t-cells. They attach opsonins to pathogens and
phagocytes.
range of diagnostic feedback from the one test. For example: important in preventing destroying it by mark them out for the attention of phagocytes. They also
• Pregnancy testing » following the implantation of the egg in the uterine wall, increased levels of hCG ( hormone autoimmune responses. direct enzyme secrete the protein interferon that limits the ability of
chorionic gonadotropin) can be detected in blood or urine. HCG antigens are detected by complementary hCG, action. viruses to replicate.
monoclonal, antibodies immobilised on the ELISA plate which forms an antigen - antibody couple and results in a
linked enzyme to produce the the characteristic colour change associated with pregnancy kits.
• Testing for viral pathogens» an ELISA plate impregnated with the viral antigens is coated with blood serum from the
patient. If the patients blood contains complementary antibodies evidence of infection) then the antigen antibody
complex triggers an enzyme reaction that leads to a colour change.
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