Immunology:
Pathogens are microorganisms that are responsible for causing disease, examples of pathogens
are: fungi, bacteria and viruses. Cells belonging naturally (the body’s own cells) are known as ‘self’,
whereas cells not belonging naturally (not the body’s own cells) are known as ‘non-self’. An antigen
is a protein that stimulates/triggers an immune response which is detected by the body. A cell that
presents antigens on its cell-surface membrane is called an antigen-presenting cell. A few
examples of antigen presenting cells are abnormal cells (cancer cells), viruses, the body’s own
infected cells and phagocytes.
Phagocytosis:
A phagocyte/macrophage is a type of white blood cell which is responsible in an immune response
called ‘phagocytosis’. A phagocyte detects and recognises a foreign pathogen entering the body,
by its foreign antigens. Protein receptors on the phagocyte are complementary to specific antigens
on foreign pathogens, when these two bind together, the phagocyte is able to fuse with the
pathogen, creating an attachment. Next, the cell membrane and cytoplasm of the phagocyte
moves around the pathogen, enclosing it in a phagosome. A lysosome fuses with the phagosome
and releases hydrolytic (digestive) enzymes which hydrolyses the pathogen. Waste products of the
pathogen are discarded and useful material remaining; e.g specific antigens of the pathogen are
presented on the cell-surface membrane of the phagocyte. The phagocyte responsible for
destroying the pathogen now becomes a specific antigen presenting cell.
Extra information: the enzymes released by lysosomes are called ‘lysosyzmes’. It works by
hydrolysing/breaking down peptidogylcan also known as murein in prokaryotic (bacteria) cell
walls.
Cell mediated immune response
T-helper cells play a signifiant role in immunity. T-helper cells are a type of immune cell which have
specific protein receptors embedded within it’s cell-surface membrane. These protein receptors on
the T-helper cells are each complementary to specific antigens on antigen presenting cells ( e.g
phagocytes after phagocytosis), which allow them to bind. Once bound together, the T-helper cell
is officially activated. T-helper cells undergo mitosis and clonal selection to produce T memory
cells, cytotoxic T cells and more T-helper cells. Each type produced through clonal selection has its
own purpose. Cytotoxic T cells kill non-self cells (e.g pathogens) directly by releasing an enzyme
called perforin, which generates gaps (pores) in the cell-membrane, so water can enter the cell
through osmosis down a water potential gradient and can cause cell lysis— eventually resulting in
bursting and cell death. T memory cells remain in the bloodstream and tissue fluid. So when the
same type of pathogen is encountered again or a re-infected cell, a secondary immune response
will be stimulated at a faster rate, destroying a pathogen before it causes disease. More T-helper
cells can be produced, as they are also involved in activation of B-cells. Therefore, more T-helper
cells present, more B-cells are activated for humoral response.
Humoral immune response:
In the humoral immune response, B cells are introduced. As mentioned previously, T helper cells
are required for the activation of B cells. When the specific protein receptors on T-helper cells
interact with complementary antigens on antigen presenting cells (phagocyte), T-helper cells
release cytokines ( which is a form of cell signalling). B cells have specific antibody receptors
embedded within its cell-surface membrane which are complementary to specific antigens on
antigen presenting cells. When bound together, it forms an antigen-antibody complex. The
cytokines released previously now successfully stimulate the B cell to divide through mitosis and
undergo clonal selection to produce two required cells; plasma cells and B memory cells. Plasma
cells secrete a mass production of monoclonal antibodies, antibodies that are specific and
complementary to a particular antigen. Antibodies destroy invading pathogens by either carrying
out agglutination or neutralisation. B memory cells remain in the bloodstream, in case the same
pathogen or a re-infected cell is encountered, so a faster antibody production is stimulated and
pathogen is destroyed before causing disease ( this will be further explained below)
Primary response:
When a specific antigen on an invading pathogen is encountered for the first time, an immune
response is stimulated— this is a primary response. A primary response is expected to be very slow
as there is a very small, limited number of T-helper and B cells present. Initially, cell mediated and
humoral response takes a longer time to occur due to this. Eventually, the body successfully
produces sufficient numbers of T-helper cells and B cells respectively, hence the body produces
enough of the required antibody to destroy the pathogen— meanwhile amongst waiting mitosis
and clonal selection of both cell mediated and humoral responses, the infected person will show
symptoms. After initial exposure and hydrolysis of the pathogens, memory T and B cells are
Pathogens are microorganisms that are responsible for causing disease, examples of pathogens
are: fungi, bacteria and viruses. Cells belonging naturally (the body’s own cells) are known as ‘self’,
whereas cells not belonging naturally (not the body’s own cells) are known as ‘non-self’. An antigen
is a protein that stimulates/triggers an immune response which is detected by the body. A cell that
presents antigens on its cell-surface membrane is called an antigen-presenting cell. A few
examples of antigen presenting cells are abnormal cells (cancer cells), viruses, the body’s own
infected cells and phagocytes.
Phagocytosis:
A phagocyte/macrophage is a type of white blood cell which is responsible in an immune response
called ‘phagocytosis’. A phagocyte detects and recognises a foreign pathogen entering the body,
by its foreign antigens. Protein receptors on the phagocyte are complementary to specific antigens
on foreign pathogens, when these two bind together, the phagocyte is able to fuse with the
pathogen, creating an attachment. Next, the cell membrane and cytoplasm of the phagocyte
moves around the pathogen, enclosing it in a phagosome. A lysosome fuses with the phagosome
and releases hydrolytic (digestive) enzymes which hydrolyses the pathogen. Waste products of the
pathogen are discarded and useful material remaining; e.g specific antigens of the pathogen are
presented on the cell-surface membrane of the phagocyte. The phagocyte responsible for
destroying the pathogen now becomes a specific antigen presenting cell.
Extra information: the enzymes released by lysosomes are called ‘lysosyzmes’. It works by
hydrolysing/breaking down peptidogylcan also known as murein in prokaryotic (bacteria) cell
walls.
Cell mediated immune response
T-helper cells play a signifiant role in immunity. T-helper cells are a type of immune cell which have
specific protein receptors embedded within it’s cell-surface membrane. These protein receptors on
the T-helper cells are each complementary to specific antigens on antigen presenting cells ( e.g
phagocytes after phagocytosis), which allow them to bind. Once bound together, the T-helper cell
is officially activated. T-helper cells undergo mitosis and clonal selection to produce T memory
cells, cytotoxic T cells and more T-helper cells. Each type produced through clonal selection has its
own purpose. Cytotoxic T cells kill non-self cells (e.g pathogens) directly by releasing an enzyme
called perforin, which generates gaps (pores) in the cell-membrane, so water can enter the cell
through osmosis down a water potential gradient and can cause cell lysis— eventually resulting in
bursting and cell death. T memory cells remain in the bloodstream and tissue fluid. So when the
same type of pathogen is encountered again or a re-infected cell, a secondary immune response
will be stimulated at a faster rate, destroying a pathogen before it causes disease. More T-helper
cells can be produced, as they are also involved in activation of B-cells. Therefore, more T-helper
cells present, more B-cells are activated for humoral response.
Humoral immune response:
In the humoral immune response, B cells are introduced. As mentioned previously, T helper cells
are required for the activation of B cells. When the specific protein receptors on T-helper cells
interact with complementary antigens on antigen presenting cells (phagocyte), T-helper cells
release cytokines ( which is a form of cell signalling). B cells have specific antibody receptors
embedded within its cell-surface membrane which are complementary to specific antigens on
antigen presenting cells. When bound together, it forms an antigen-antibody complex. The
cytokines released previously now successfully stimulate the B cell to divide through mitosis and
undergo clonal selection to produce two required cells; plasma cells and B memory cells. Plasma
cells secrete a mass production of monoclonal antibodies, antibodies that are specific and
complementary to a particular antigen. Antibodies destroy invading pathogens by either carrying
out agglutination or neutralisation. B memory cells remain in the bloodstream, in case the same
pathogen or a re-infected cell is encountered, so a faster antibody production is stimulated and
pathogen is destroyed before causing disease ( this will be further explained below)
Primary response:
When a specific antigen on an invading pathogen is encountered for the first time, an immune
response is stimulated— this is a primary response. A primary response is expected to be very slow
as there is a very small, limited number of T-helper and B cells present. Initially, cell mediated and
humoral response takes a longer time to occur due to this. Eventually, the body successfully
produces sufficient numbers of T-helper cells and B cells respectively, hence the body produces
enough of the required antibody to destroy the pathogen— meanwhile amongst waiting mitosis
and clonal selection of both cell mediated and humoral responses, the infected person will show
symptoms. After initial exposure and hydrolysis of the pathogens, memory T and B cells are
