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2609002
IMMUNITY
Description
Defence mechanisms, phagocytosis, cell-mediated response, humoral response
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as biology
a level
Mind Map by
Ashiana Fraser
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Created by
Ashiana Fraser
about 9 years ago
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Resource summary
IMMUNITY
Defence mechanisms
Non-specific
Physical barrier
Skin, mucus, HCl
Phagocytosis
Specific
Cell-mediated
T-Cells
Humoral
B-Cells
Specific and non-specific mechanisms
Non-specific
Don't distinguish between pathogens
Act immediately
Specific
Do distinguish between pathogens
Slower but provide long-lasting immunity
How lymphocytes recognise their own cells
There are around 10 million different lymphocytes,each capable of recognising a different chemical shape
ie having a protein on it's surface that is complementary to one of the proteins on the pathogen
In the fetus, these lymphocytes are constantly colliding with other cells
Infection in the fetus is rare because it is protected from the outside world be the mother and in particular the placenta
Lymphocytes will therefore collide almost exclusively with the body's own cells
Some of the lymphocytes will have receptors that exactly fit those of the body's own cells
These lymphocytes either die or are supressed
The only remaining lymphocytes are those that fit foreign material and therefore only respond to foreign material
Phagocytosis
Large particles - such as bacteria - are too big to cross cell-surface membranes by diffusion or active transport
Instead they are engulfed by cells in the form of vesicles
The phagocyte is attracted to the pathogen by chemoattractants. It moves towards the pathogen along a concentration gradient
The phagocyte binds to the pathogen
Lysosomes within the phagocyte migrate towards the phagosome formed by engulfing the bacterium
The lysosomes release their lytic enzymes into the phagosome, where they break down the bacterium
The breakdown products of the bacterium are absorbed by the phagocyte
Causes inflammation at the site of infection
The swollen area contains dead pathogens and phagocytes (pus)
Inflammation is the result of the release of histamine - causes dilation of the blood vessels
This speeds up the delivery of phagocytes to the site of infection
Cell-mediated immunity (T cells)
T lymphocytes mature in the thymus gland
They can distinguish invader cells from normal cells because:
After phagocytosis, the phagocytes present some of the antigens of the pathogen on their own cell surface membrane
Body cells invaded bt a virus present some of the viral antigens on their own cell-surface membranes as a sign of distress
Cancer cells also present antigens on their cell surface membrane
These cells are ANTIGEN-PRESENTING CELLS
T lymphocytes will only respond to antigens attached to a body cell
Pathogens invade body cells or are taken in by phagocytes
The phagocyte places antigens from the pathogen on its cell surface membrane
Receptors on certain T helper cells fit exactly onto these antigens
This activates other T cells to divide rapidly by mitosis and form a clone
The cloned T cells:
Develop into memory cells that enable a rapid response to future infections
Stimulate phagocytes to engulf pathogens by phagocytosis
Stimulate B cells to divide
Kill infected cells
The role of the receptors on the T cells is important
The receptors on each T cell respond to a single antigen
There are a vast number of different types of T cell, all responding to a different antigen
How T cells kill infected cells
Produce a protein that makes a hole in the cell surface membrane
The holes mean the cell becomes freely permeable to all substances and dies as a result
The action of T cells is most effective against viruses - viruses live and reproduce inside living cells
Humoral immunity (B cells(
Involves antibodies (soluble in tissue fluid and blood aka humor)
There are 10 million types of B cells, each type producing a different antibody that responds to one specific antigen
The specific antibody attaches to the complementary antigen and the B cell that produces this antibody divides by mitosis
This forms clones of identical B cells that all produce the antibody that is specific to the antigen of the foreign cell
One pathogen has many different proteins on its surface - all of which act as antigens
Toxins produced by a pathogen also act as antigens
Therefore many different B cells make clones. The clones develop into one of two types of cell:
Memory cells
Live for decades
Circulate in the blood and tissue fluid
When they encounter the same antigen again, they divide rapidly and develop into plasma cells and more memory cells
Plasma cells produce the antibodies needed to destroy the pathogen
SECONDARY IMMUNE RESPONSE
More rapid and of greater intensity than primary response
New infection is repulsed before it can cause any harm
Role of B cells
Surface antigens on the invading pathogen are taken up by B cells
The B cells process the antigens and present them on their surfaces
T helper cells attach to the processed antigens on the B cells and activate them
B cells are now activated to divide by mitosis to give a clone of plasma cells
The cloned plasma cells produce antibodies that exactly fir the antigens on the pathogens surface
The antibodies attach to the antigens on the pathogen and destroy them
Some B cells develop into memory cells that can quickly respond to future infections
Plasma cells
Secrete antibodies
Antibodies destroy pathogens and toxins
Last for a few days
Responsible for the immediate defense of the body against infection
PRIMARY IMMUNE RESPONSE
Antigenic variability
Some pathogens have many different strains, each with different antigens. These strains, and so the anitgens, are always changing
Any subsequent infections are therefore likely to be caused by a different variety of the pathogen
Their antigens will not correspond to the antibodies of the memory cells formed in the first infection
The body acts as if each infection is a new one and the reaction is much slower - in which time we develop symptoms
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