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IMMUNITY

Mind map: Immunity
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IMMUNITY
Defence mechanisms
- Non-specific
- Physical barrier
- Skin, mucus, HCl
- Phagocytosis
- Physical barrier
- Specific
- Cell-mediated
- T-Cells
- Humoral
- B-Cells
- Cell-mediated
- Non-specific
Specific and non-specific mechanisms
- Non-specific
- Don't distinguish between pathogens
- Act immediately
- Don't distinguish between pathogens
- Specific
- Do distinguish between pathogens
- Slower but provide long-lasting immunity
- Do distinguish between pathogens
- Non-specific
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
- These lymphocytes either die or are supressed
- Some of the lymphocytes will have receptors that exactly fit those of the body's own cells
- Lymphocytes will therefore collide almost exclusively with the body's own cells
- Infection in the fetus is rare because it is protected from the outside world be the mother and in particular the placenta
- There are around 10 million different lymphocytes,each capable of recognising a different chemical shape
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
- The lysosomes release their lytic enzymes into the phagosome, where they break down the bacterium
- Lysosomes within the phagocyte migrate towards the phagosome formed by engulfing the bacterium
- The phagocyte binds to the pathogen
- 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
- Large particles - such as bacteria - are too big to cross cell-surface membranes by diffusion or active transport
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
- Cancer cells also present antigens on their 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
- After phagocytosis, the phagocytes present some of the antigens of the pathogen on their own cell surface membrane
- They can distinguish invader cells from normal cells because:
- 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
- The receptors on each T cell respond to a single antigen
- The cloned T cells:
- This activates other T cells to divide rapidly by mitosis and form a clone
- Receptors on certain T helper cells fit exactly onto these antigens
- The phagocyte places antigens from the pathogen on its cell surface membrane
- Pathogens invade body cells or are taken in by phagocytes
- 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
- The holes mean the cell becomes freely permeable to all substances and dies as a result
- Produce a protein that makes a hole in the cell surface membrane
- T lymphocytes mature in the thymus gland
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
- The antibodies attach to the antigens on the pathogen and destroy them
- The cloned plasma cells produce antibodies that exactly fir the antigens on the pathogens surface
- B cells are now activated to divide by mitosis to give a clone of plasma cells
- T helper cells attach to the processed antigens on the B cells and activate them
- The B cells process the antigens and present them on their surfaces
- Surface antigens on the invading pathogen are taken up by B cells
- Role of B cells
- SECONDARY IMMUNE RESPONSE
- Plasma cells produce the antibodies needed to destroy the pathogen
- 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
- Secrete antibodies
- Memory cells
- Therefore many different B cells make clones. The clones develop into one of two types of cell:
- Toxins produced by a pathogen also act as antigens
- One pathogen has many different proteins on its surface - all of which act as antigens
- This forms clones of identical B cells that all produce the antibody that is specific to the antigen of the foreign cell
- The specific antibody attaches to the complementary antigen and the B cell that produces this antibody divides by mitosis
- 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
- Their antigens will not correspond to the antibodies of the memory cells formed in the first infection
- Any subsequent infections are therefore likely to be caused by a different variety of the pathogen
- Some pathogens have many different strains, each with different antigens. These strains, and so the anitgens, are always changing
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- Description
- Defence mechanisms, phagocytosis, cell-mediated response, humoral response
- Created by
- Ashiana Fraser
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