absorbed into the cytoplasm of phagocyte.

Lytic enzymes hydrolyse,destroy and digest pathogen of which soluble products are
Lysosomes migrate towards phagosome and release their lytic enzymes.
a phagosome.
Part of cell-surface membrane of phagocyte is used to contain ingested pathogen within
Phagocytes form a gulf around pathogen and then engulfs the pathogen.
and attach themselves to surface of pathogen.
Phagocytes attracted by toxins/chemicals pathogen secretes known as chemoattractants
to the site of infection.
Histamine is released causing dilation of blood vessels speeding up arrival of phagocytes

Phagocytosis involves phagocytes (a type of white blood cell) and the process is as follows:
Phagocytosis: A non specific mechanism that responds rapidly to infection from pathogens.

6.2 Phagocytosis
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6.1 Defence Mechanisms

Defence Mechanisms: Protect us from pathogens which cause disease; this is either from
secretion of harmful toxins or from infecting and damaging host cells.

Non-specific: Mechanisms that do not distinguish from one type of pathogen from another, so
responds to all in the same way. These include barriers to entry of pathogens and phagocytosis
and respond rapidly. Example of barriers:

Skin - provides a physical barrier that pathogens cannon penetrate.

Epithelia covered in mucus - goblet cells secrete mucus, pathogens stick to mucus, cilia
move pathogens up trachea to be swallowed into stomach.
Hydrochloric acid in stomach - Low PH denatures enzymes of pathogens, leading to
pathogens being destroyed.

Specific: Mechanisms that do distinguish from one type of pathogen from another. The responces
are less rapid but give long-lasting immuniy. This comes in the form of: cell-mediated responses
involving T-cells and humoral responses involving B-cells.
phagocytosis (c) stimulate B-cells to divide (d) Kill infected cells.
future infections by same pathogen (b) Stimulate phagocytes to engulf pathogens by
The cloned T cells : (a) Develop into shape-memory cells for rapid responce to
Activates T-cells to divide rapidly by mitosis and form a clone.
Receptors on certain T-cells fit exactly onto antigens.
Antigens from pathogen displayed on cell surface membrane.
Pathogen invade body cells or taken in by phagocytes.
presenting cells.
Cell-mediated immunity: A specific mechanism where T-lymphocytes respond to antigen-
T Lymphocytes: Mature in Thymus gland and associated with cell-mediated immunity.
stimulates the production of antibodies.
Antigens: A protein that is recognised as non-self stimulating an immune responce. This
6.3 T cells and cell-mediated immunity
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6.4 B cells and humoral immunity
B-Lymphocytes: Mature in Bone marrow and involved in humoral immunity.
Humoral Immunity: A specific mechanism where antigen presenting B-cells are activated by t-
cells to carry out humoral immunity and the process is as follows:
Antigens on surface of pathogen is taken up by B-cells.
B cells process the antigen and present them on their surface.
T-helper cells attach to the displayed antigen on B-cells activating the B-cells.
B-cells activiated to divide by mitosis to give a clone of plasma cells.
Cloned plasma cells produce antibodies that are specific to the shape of antigens on
pathogen's surface.
Primary immune responce is that antibodies attach or bind to antigen on pathogen forming
an antigen-anitbody-complex, destroying pathogen.
Secondary responce is a result of some B-cells developing into shape memory cells.
Divides rapidly into plasma cells that produce antibodies.
means of administering vaccine, means of producing/transporting/storing vaccine.
Successful Vaccination Programme: Economically viable, few side-effects, herd immunity,
Generally long-lasting.
Active Immunity: Stimulating production of antibodies by individuals own immune system.
therefore not replaced by individual and eventually broken down by body. Generally short-lived.
Passive Immunity: Produced by introduction of antibodies to individuals from an outside source,
pathogen causes disease.
secondary infection to produce antibodies that bind to pathogen antigen and destroys them before
shape-memory cells. This gives immunity to pathogen as shape memory cells divide rapidly during
the antigen of a pathogen that stimulates an immune responce. This stimulates production of
Vaccination: Injecting an individual with a weakened/attenuated form of a pathogen containing
6.6 Vaccination
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6.5 Antibodies
Antigenic Variability: Describes the shape of antigens of a pathogen as constantly changing.
Thesefore new strain causes disease as antibodies from previouse infection do not compliment
shape of antigen of the new strain. Cannot respond to infection by secondary responce, so must
use primary responce.
Antibodies: Synthesised by B-cells, and are very specific in shape to bind to a specific antigen
shape. Antibodies are made up of four polypeptide chains so is a quaternary structure. Antibodies
bind to complimentary antigen to form an antigen-antibody-complex Antibodies have a variable
region, made up of a speicific sequence of amino acids that make up the 3-D tertiary shape. Also
has a constant region that is the same in all antibodies that bonds to receptors on B-cells.
Monoclonal Antibodies: The cloning of a single type of antibody outside of the body. Can be used
in cancer treatment, transplant surgery, imunoassay and sepearation of a chemical from a mixture.
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6.6 Vaccination
Why vaccination does not eliminate disease: Fails to induce immunity in people with defective
immune systems. May develop disease immediately after vaccination but before immunity levels
are high enough to prevent infection. Mutations of pathogen causes antigenic variability e.g.
influenza changes its antigen shape frequently. Many strains of a particular pathogen so cannot
develop vaccine against all. Individuals object to vaccination.
Problems with controlling cholera:
Intestinal disease so not easily reached by immune system or antibiotics.
Antigen of cholera pathogen changes rapidly (antigenic variability).
Mobile populations spread cholera.
Problems with controlling TB:
Increase in HIV infection so more people with impaired immune systems.
Poverty, wars, political unrest create breeding grounds for TB e.g. refugee camps.
Proportion of elderly people in population increasing, as these people have a less effective
or weakened immune system.
Mobile populations so difficult to ensure individuals are vaccinated.