Post on 17-Dec-2015
What You Should Know
• Immune surveillance • A range of white blood cells constantly circulate
monitoring the tissues. • If tissues become damaged or invaded, cells release
cytokines which increase blood flow resulting in specific white blood cells accumulating at the site of infection or tissue damage.
• Clonal selection theory. • Lymphocytes have a single type of membrane receptor
specific for one antigen. • Antigen binding leads to repeated lymphocyte division
resulting in a clonal population of lymphocytes. •
Immune Surveillance• A range of different types of
white blood cells continuously circulate in the blood monitoring the state of the tissues
• If damage is detected some of these white blood cells release cytokines into the blood
• This attracts large numbers of phagocytes and T cells to the damaged or infected area
• Often white blood cells squeeze through the pores in the capillaries to gain access to the tissue
Lymphocytes on patrolWhite blood cells, calledlymphocytes, move through thebloodstream alongside red blood
cells.
Clonal Selection Theory
• Any foreign molecule that is able to elicit a specific response from the immune system is referred to as an antigen
• Viruses, bacteria, toxins etc.
• The body has an enormous number of different lymphocytes
(continued…)• Each lymphocyte has a
single type of antigen receptor on the surface of its membrane
• The antigen receptor is specific for one antigen
• Each lymphocyte is able to attach to and be activated by one type of antigen
(continued…!)
• The lymphocyte then divides repeatedly to form a clonal population of identical lymphocytes
• This is called clonal selection
What You Should Know• Lymphocytes respond specifically to antigens on foreign cells, cells infected by pathogens and
toxins released by pathogens. • T-lymphocytes have specific surface proteins that allow them to distinguish between the
surface molecules of the body’s own cells and cells with foreign molecules on their surface. • Immune system regulation failure leads to T-lymphocyte immune response to self antigens
(auto immune disease). • Allergy is a hypersensitive B- lymphocyte response to an antigen that is normally harmless• T-lymphocytes • One group of T-lymphocytes destroy infected cells by inducing apoptosis. • Another group of T-lymphocytes secrete cytokines that activate B lymphocytes and
phagocytes. • When pathogens infect tissue, some phagocytes capture the pathogen and display fragments
of its antigens on their surface. • These antigen presenting cells activate the production of a clone of T-lymphocytes that move
to the site of infection under the direction of cytokines. • B-lymphocytes • Each B-lymphocyte clone produces a specific antibody molecule that will recognise a specific
antigen surface molecule on a pathogen or a toxin. • Antigen-antibody complexes may inactivate a pathogen or toxin or render it more susceptible
to phagocytosis. • In other cases the antigen-antibody complex stimulates a response which results in cell lysis. • B-lymphocytes activated by antigen presenting cells and T-lymphocytes produce a clone of B-
lymphocytes that secrete antibodies into the lymph and blood where they make their way to the infected area.
Lymphocytes• Every individual has a unique
‘antigen signature’• It is vital that a person’s
lymphocytes do not regard the person’s cell surface proteins as antigens and attack them
• Lymphocytes respond specifically to – antigens on foreign cells – cells infected by pathogens – toxins released by pathogens
T Lymphocytes• T-lymphocytes have
specific surface proteins that allow them to distinguish between the surface molecules of the body’s own cells and cells with foreign molecules on their surface
• ‘self’ molecules on the surface- no action
• ‘non-self’ molecules- immune response initiated
Those lymphocytes that bind to antigens from the body's own tissues are destroyed
Auto Immune Disease• The failure to recognise self-antigens can result
in autoimmune disease
• The T lymphocytes attack the body’s own cells
• Examples include– Type 1 diabetes– Rheumatoid arthritis– Multiple sclerosis– Celiac disease (see textbook for more detail)
Allergy• An allergy is a hypersensitivity disorder of the immune
system• Sometimes the immune system over reacts to
harmless substances e.g. pollen, dust.• When the immune system over reacts B lymphocytes
are activated producing antibodies which attach to the mast cells in the connective tissue causing the release of histamine
• Excessive histamine stimulates the inflammatory response
T Lymphocytes(2 types)
• 1. Cytotoxic T cells (TC) destroy infected cells by inducing apoptosis
• 2. Helper T (TH) cells secrete cytokines that activate phagocytes, cytotoxic T cells and B lymphocytes
Antigen Presenting Cell• After a phagocyte destroys an
invading pathogen it presents fragments of its antigens on its cell surface
• The phagocyte is now referred to as an antigen presenting cell
• A specific helper T cell then binds to the antigen on the antigen presenting cell
• The helper T cell becomes activated and produces a clone of activated helper cells
• The helper T cells secrete cytokines which activate B cells to secrete antibodies and macrophages to destroy ingested microbes. They also activate cytotoxic T cells to kill infected target cells.
B Lymphocytes• B-lymphocytes activated by
antigen presenting cells and T-lymphocytes produce a clone of B-lymphocytes that secrete antibodies into the lymph and blood where they make their way to the infected area
• Each B-lymphocyte clone produces a specific antibody molecule that will recognise a specific antigen surface molecule on a pathogen or a toxin.
The Action of B Lymphocyte
• Antigen-antibody complexes may inactivate a pathogen or toxin or render it more susceptible to phagocytosis
The Action of B Lymphocyte
• In other cases the antigen-antibody complex stimulates the activation of proteins which result in cell lysis
What You Should Know
• Immunological memory. • Some T- and B-lymphocytes produced in
response to antigens by clonal selection survive long-term as memory cells.
• A secondary exposure to the same antigen rapidly gives rise to a new clone of lymphocytes producing a rapid and greater immunological response.
Immunological Memory• Towards the end of each battle to
stop an infection, some T-cells and B-cells turn into Memory T-cells and Memory B-cells
• These cells remember the virus or bacteria they just fought
• These cells live in the body for a long time, even after all the viruses from the first infection have been destroyed
• They stay in the ready-mode to quickly recognize and attack any returning virus or bacteria
Secondary Response• The first time your body fights a
virus, it can take up to 15 days to make enough antibodies to get rid of it
• With the help of Memory B-cells, the second time your body sees that virus, it can do the same in thing 5 days
• It also makes 100 times more antibodies than it did the first time
• The faster your body makes antibodies, the quicker the virus can be destroyed
• With the help of Memory B-cells, you might get rid of it before you even feel sick
• This is called gaining immunity