McKenna's Pharmacology for Nursing, 2e - page 245

C H A P T E R 1 5
 Introduction to the immune response and inflammation
233
would start to leak out of the capillaries (often this can
be heard as rales); the person would complain of chest
discomfort; and the increased blood flow to the area of
infection would make it appear hot or very active on a
scan. No matter what the cause of the insult, the body’s
local response is the same.
Once the inflammatory response is under way and
neutrophils become active, engulfing and digesting
injured cells or the invader, they release a chemical that
is a natural
pyrogen
, or fever-causing substance. This
pyrogen resets specific neurons in the hypothalamus to
maintain a higher body temperature, seen clinically as a
fever. The higher temperature acts as a catalyst to many
of the body’s chemical reactions, making the inflam­
matory and immune responses more effective. Treating
fevers remains a controversial subject because lowering a
fever decreases the efficiency of the immune and inflam­
matory responses.
The leukotrienes (autocoids activated through the
kinin system) affect the brain to induce slow-wave
sleep, which is believed to be an important energy con­
servation measure for fighting the invader. They also
cause myalgia and arthralgia (muscle and joint pain)—
common signs and symptoms of various inflammatory
diseases—which also cause reduced activity and save
energy. All of these chemical responses make up the
total clinical picture of an inflammatory reaction.
The immune response
More specific invasion can stimulate a more specific
response through the immune system. As mentioned
previously, stem cells in the bone marrow produce
lymphocytes that can develop into T lymphocytes (so
named because they migrate from the bone marrow
to the thymus gland for activation and maturation) or
B lymphocytes (so named because they are activated in
the bursa of Fabricius in chickens, although the specific
point of activation in humans has not been identified).
Other identified lymphocytes include natural killer cells
and lymphokine-activated killer cells. Both of these cells
are aggressive against neoplastic or cancer cells and
promote rapid cellular death. They do not seem to be
programmed for specific identification of cells.
Nutritional:
Immune: Immune response
Research in the area of lymphocyte identification
is relatively new and continues to grow. There may be
other lymphocytes with particular roles in the immune
response that have not yet been identified.
T cells
T cells
are programmed in the thymus gland and provide
what is called cell-mediated immunity (Figure 15.3).
T cells develop into at least three different cell types.
1.
Effector or cytotoxic T cells
are found throughout
the body. These T cells are aggressive against non-self
cells, releasing cytokines, or chemicals, that can
either directly destroy a foreign cell or mark it for
aggressive destruction by phagocytes in the area via
an inflammatory response. These non-self cells have
membrane-identifying antigens that are different
from those established by the person’s MHC. They
may be the body’s own cells that have been invaded
by a virus, which changes the cell membrane;
neoplastic cancer cells; or transplanted foreign cells.
2.
Helper T cells
respond to the chemical indicators of
immune activity and stimulate other lymphocytes,
including B cells, to be more aggressive and responsive.
3.
Suppressor T cells
respond to rising levels of
chemicals associated with an immune response to
suppress or slow the reaction. The balance of the
helper and suppressor T cells allows for a rapid
response to body injury or invasion by pathogens,
which may destroy foreign antigens immediately and
then be followed by a slowing reaction if the invasion
continues. This slowing allows the body to conserve
energy and the components of the immune and
inflammatory reaction necessary for basic protection
and to prevent cellular destruction from a continued
inflammatory reaction.
B cells
B cells
are found throughout the MPS in groups called
clones. B cells are programmed to identify specific
proteins or antigens. They provide what is called humoral
immunity (Figure 15.4). When a B cell reacts with its
specific antigen, it changes to become a plasma cell.
Plasma cells produce
antibodies
, or immunoglobulins,
which circulate in the body and react with this specific
antigen when it is encountered. This is a direct chemical
reaction. When the antigen and antibody react, they
NON-SELF CELL
Cytotoxic T cell
Release of cytokines
Memory cytotoxic
T cells
Stimulated by helper T cells
Inhibited by suppressor T cells
Death of non-self cell
FIGURE 15.3 
Cell-mediated immune response. Cytotoxic
T cells are activated when recognising a non-self cell.
Memory T cells are formed. Cytokines are released to
destroy the non-self cell.
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