8.2 Fighting back
4. Explain how bacteria and viruses can disrupt regular cellular or body function.
5. Explain how immune systems respond to infections.
2. Specific immunity (specific pathogens are recognized as foreign by lymphocytes and
Third line of defense: Immune and lymphatic system
Lymph moves invaders from the
sites of infection into lymph nodes
where they are attacked by masses
of white blood cells. This is why
your lymph nodes ie in your neck
can swell up when you are sick
Besides macrophages and natural
killer cells which are non-specific,
lymph contains some lymphocytes
called B cells and T cells which
provide specific protection.
Note: on the importance of cell surface proteins
Proteins are found on the surface of virtually all cells and
serve very many functions.
Receptor proteins are used by cells to sense and
respond to incoming signals ie “Grow in this direction”
“Ouch!” “Take in more potassium ions” “Work harder”
“Turn on gene X” “Beware of invaders” “Die!”
A ligand is what binds to a receptor to signal it. Two
receptor proteins(R) with bound ligands (L) are shown on
the left. Only 1 ligand binds to1 receptor as a rule. They
act like lock-and-key. There are many different types
of cells in your body with different
receptors. As well, cells in different species have different cell surface receptor proteins. There are 1000s of
different locks and keys.
The way immune system cells and antibodies work is by
recognizing foreign substances called antigens. The cells
of your immune system recognize the proteins on the
surface of your own cells as being “self” and leave them
alone. Any shape on an antigen that is recognized as
foreign (non-self) is attacked by the immune system.
Antigens could be dust, bacteria, viruses, or toxins.
Questions: 1. How do prions evade the immune system?
2. What has gone wrong with the immune system when a person has an auto-immune disease?
Three major players in your immune system which detect antigens are: antibodies, B cells and T cells
Antibodies are specialized proteins secreted by B cells. Antibodies recognize and bind to
antigens. One antibody recognizes one epitope (specific shape). One antigen may be made
up of several epitopes (shapes). The specificity of one particular antibody recognizing one
antibodies particular epitope is another lock and key relationship.
Antibodies can cause foreign bacterial cells to
clump together which makes it easier for
phagocytes to capture them. Antibodies can
also stimulate another feature of the immune
system: the complement system
(mentioned in the 2nd line of defense) where
specific proteins attach to the surface of the
foreign cell, punch holes in its plasma
membrane causing it to rupture.
Both B and T cells are types of lymphocytes or white blood cells initially produced in bone marrow. Both
have receptors on their surface to recognize epitopes (specific shapes). One cell only makes one type
of receptor that recognizes one epitope. The receptors on their cell surface are basically antibodies that
remain attached in their cell membrane.
B cells secrete antibodies that, as T cells directly bind and kill to host
mentioned, recognize and bind to cells that are cancerous or have been
invading cells making the infected by viruses. They can also go
pathogenic cells clump together after larger invaders like parasitic
before macrophages can attack T cells worms or fungal cells.
them. T cells also assist the work of B cells.
Because one B cell or T cell also only recognizes and binds to one
epitope, at any one time your body is making thousands of B cells, T cells
and antibodies to be able to recognize thousands of potential foreign
Question: 3. Why are organ transplants possible, if the body attacks anything it perceives as foreign?is
Any B or T cell that recognizes an epitope found on a host (self) cell
destroyed before the cells are mature so that the immune system does
not attack cells in the host’s own body.
During an infection, thousands of copies are http://altered-states.net/barry/newsletter168/antigens4.gif recognize the
Figure from: made of the B and/or T cells which specific
antigens on the pathogen. Thousands of the correct antibodies are also made to fight the infection.
In addition to producing cells actively involved in fighting the infection, extra copies of the specific B and T
cells (which recognized the antigen) are made called memory cells. Once the infection lessens the production
of antibodies and white blood cells slows down, however the memory cells persist in the body after the
infection is over.
These memory cells allow the immune system to respond very quickly if the pathogen is re-encountered.
During a second encounter they can divide so quickly and attack the pathogen so fast that you likely will not
get sick a second time.
When an antigen is first encountered it takes the immune
system some time before it produces a significant amount
of antibodies and white blood cells to fight the infection.
These are the “primary responses” shown on the graph.
Antigen X is re-encountered at the time point shown by the
arrow is on the graph. Because of the persisting memory
cells, antibodies and white blood cells are produced more
quickly and at higher concentration than if it was the first
time they had been encountered. We call this acquired
immunity. The host likely does even develop any
symptoms of illness because of the faster response.
Viruses can only bind to cells where their surface proteins can bind to receptors on a cell’s surface. This is
what tends to make viruses have such specific host ranges.
Egs. the HIV virus bind and infect helper T cells in your immune
Cauliflower mosaic virus bind and infect leaf cells of plants in the
Broccoli family (which includes cauliflower)
Adenoviruses cells of our respiratory tract (and often only part of
the tract which is why different viruses give us different varieties of
Example of how a virus uses its receptors to infect a cell: The influenza virus
has specialized proteins on its surface like hemagglutinin which binds to a specific
type of sugar molecule (sialic acid) found on glycoproteins of some cells. Once the
virus binds to this sugar this stimulates the host cell to engulf the virus by
endocytosis. The cell attempts to digest the virus by turning the vesicle into a
lysosome (low pH, many enzymes to breakdown whatever is inside). The
hemagglutinin protein refolds into a new shape in the low pH environment and
reacts with the lysosomal membrane to allowing the viral genome to exit into the
Why do we keep getting colds and flus?
Mutations can change what proteins viruses have on their surface these new proteins are no longer
recognized by a person’s immune system.
Cold and flu virus genomes are made of RNA rather than DNA. RNA mutates much more frequently than
DNA This means that cold and flu viruses are changing from year to year.
Regular flu shots contains fragmented viruses from last year’s flu viruses. If this year’s flu strains have
changed too much compared to last year’s you may still catch the flu. The H1N1 flu shot contains fragmented
(dead) pieces of the H1N1 virus.
Questions: 4. What part of the deactivated flu viruses are in the flu shot –the genetic material or the
capsule? Why was this part chosen?
5. A vaccine against any cellular pathogen uses dead fragmented cell walls and membranes. If the process of
fragmenting the cells is too destructive the vaccine may not be effective. Why not?
Bacterial and protist infections
Bacterial and protist cells, like viruses, are recognized as foreign by the presence of epitopes on their cell
surface. As explained earlier antibodies (and possibly T cells) work together with macrophages and
complement proteins to kill foreign cellular pathogens.
Do bacteria and protists recognize specific cells like viruses do?
More commonly they release toxins which make us sick, and they obtain energy and multiply in one particular
part of the body (site of infection or environment they can tolerate).
Fighting Infections with Antibiotics: These are drugs which can kill cellular (not viral) pathogens.
Antibiotics target cellular components or processes which are different from the host.
The first antibiotic discovered was a chemical (penicillin) made by a
fungus to kill a bacterium which was competing for the same food
source. Penicillin binds to the sugar peptidoglycan in the cell walls
of gram-positive bacteria. This weakens the cell walls causing the
cells to burst. Fungi produce a number of natural antibiotics against
bacteria. In every case the antibiotic targets some structure or
process in the bacterial cell that is not shared by fungi. If you want
to become an antibiotic designer you need to be a good cell
biologist and study what is different between the host cells and
Figure from: http://www.socialfiction.org/img/penicillin_1.jpg
Some common targets of bacterial antibiotics are:
–their cell walls or enzymes used to synthesize their cell walls causing the cells to stop dividing or to burst
(as with penicillin)
–unique bacterial components of their ribosomes shutting down their ability to make proteins causing
their cells to shut down and die
Questions: 6.Bacteria have an enzyme that allows them to synthesize folic acid from scratch. Folic acid is
used in all cells to make nucleotides, the building blocks of DNA and RNA. We lack the enzyme that bacteria
have to make folic acid, so instead we must get folic acid from the food we eat. Could we make an antibiotic
that inhibits the folic acid synthesizing enzyme in bacteria or would it harm us?
Sulfa – antibiotics (lots of people get sick when they take sulfa. May be do to shape and foreign stuffs.
a. Yes we could make and then use such an antibiotic because we lack this enzyme
b. No because we lack the enzyme we would make antibodies to both the unknown enzyme and the
antibiotic against it causing an allergic reaction.
7. Although there are some antibiotics against protists
like Giardia lamblia and Trichomonas vaginalis, it is
generally harder to find antibiotics against protists and
there is often a greater chance that some of these
antibiotics may make people sick. Considering what you
know about protist cells why might this be?
Giardia lamblia Trichomonas vaginalis
A fungus Epidermophyton floccosum which causes athletes foot is shown at
8. If you were going to try to develop an antibiotic to treat a fungal
infection, what might you target? Hint: how do fungal cells different from