C H A P T E R 1 5
Introduction to the immune response and inflammation
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• IgE is present in small amounts and seems to be
related to allergic responses and to the activation of
mast cells.
• IgD is another identified immunoglobulin whose role
has not been determined.
This process of antibody formation, called acquired
or active immunity, is a lifelong reaction. For example,
a person exposed to chickenpox will have a mild res
piratory reaction when the virus (varicella) first enters
the respiratory tract. There will then be a 2- to 3-week
incubation period as the body is forming IgM anti
bodies and preparing to attack any chickenpox virus
that appears. The chickenpox virus enters a cell and
multiplies. The cell eventually ruptures and ejects more
viruses into the system. When this happens, the body
responds with the immediate release of antibodies, and a
full scale antigen–antibody response is seen throughout
the body. Fever, myalgia, arthralgia and skin lesions are
all part of the immune response to the virus. Once all
of the invading chickenpox viruses have been destroyed
or have entered the CNS to safely hibernate away from
the antibodies, the clinical signs and symptoms resolve.
(Varicella can enter the CNS and stay dormant for many
years. The antibodies are not able to cross into the CNS,
and the virus remains unaffected while it stays there.)
The B memory cells will continue to make a supply of
immunoglobulin, IgG, for use on future exposure to the
chickenpox virus. That exposure does not usually evolve
into a clinical case because the viruses are destroyed
immediately on entering the body and do not have a
chance to multiply. Older people with weakened immune
systems, people who are immunosuppressed and indi
viduals who have depleted their immune system fighting
an infection are at risk for development of shingles if
they had chickenpox earlier in their lives. The dormant
virus, which has aged and changed somewhat, is able to
leave the CNS along a nerve root because the immuno
suppressed body is slow to respond. The antibodies do
eventually respond to the varicella, and the signs and
symptoms of shingles occur as the virus is attacked along
the nerve root. Figure 15.5 outlines this entire process.
B clones cluster in areas where they are most likely
to encounter the specific antigen that they have been
programmed to recognise. For example, pathogens or
antigens that are introduced into the body via the res
piratory tract will meet up with the B cells in the tonsils
and upper respiratory tract; antigens that enter the body
through the GI tract will meet their B cells situated in
the oesophagus and GI tract. Theorists believe that the
B cells are programmed genetically and are formed by
the time of birth. Clones of B cells contain similar cells.
The introduction of an antigen to which there are no pre
programmed B cells could result in widespread disease
because the body would have no way of responding.
A major concern about space travel has always been the
introduction of a completely new antigen to Earth; for
this reason, long periods of decontamination have been
used after rocks or debris are brought back to Earth.
Germ warfare research is ongoing in some countries to
develop an antigen that has not been seen before and to
which people would have no response.
Other mediators
Several other factors also play an important role in the
immune reaction.
Interferons
are chemicals that are
secreted by cells that have been invaded by viruses and
possibly by other stimuli. The interferons prevent viral
replication and also suppress malignant cell replication
and tumour growth.
Interleukins
are chemicals secreted by active leuco
cytes to influence other leucocytes. Interleukin 1 (IL-1)
stimulates T and B cells to initiate an immune response.
IL-2 is released from active T cells to stimulate the pro
duction of more T cells and to increase the activity of
B cells, cytotoxic cells and natural killer cells. Interleu
kins also cause fever, arthralgia, myalgia and slow-wave
sleep induction—all things that help the body to conserve
energy for use in fighting off the invader. Several other
factors released by lymphocytes and basophils have
been identified. These include interleukins such as B-cell
growth factor, macrophage-activating factor, macrophage
inhibiting factor, platelet-activating factor, eosinophil
chemotactic factor and neutrophil chemotactic factor.
The thymus gland also releases a number of
hormones that aid in the maturation of T cells and that
circulate in the body to stimulate and communicate with
T cells. Thymosin, a thymus hormone that has been rep
licated, is important in the maturation of T cells and
cell-mediated immunity. Research is ongoing on the use
of thymosin in certain leukaemias and melanomas to
stimulate the immune response.
Tumour necrosis factor (TNF), a cytokine, is a
chemical released by macrophages that inhibits tumour
growth and can actually cause tumour regression. It
also works with other chemicals to make the inflam
matory and immune responses more aggressive and
efficient. Research is ongoing to determine the thera
peutic effectiveness of TNF. TNF receptor sites are now
available for injection into people with acute rheumatoid
arthritis. These receptor sites react with TNF released
by the macrophages in this inflammatory disease. All
of these chemicals act as communication factors within
the immune system, allowing the coordination of the
immune response.
Interrelationship of the immune and inflammatory
responses
The immune and inflammatory responses work together
to protect the body and to maintain a level of homeo
stasis. Helper T cells stimulate the activity of B cells and
