Host Defense Mechanisms: An Overview

Christine Grady

E VERY MINUTE our bodies are beseiged by

invisible enemies that could cause great
harm. Fortunately, we have a complex, highly in-
to 1,000 per day.’ Through immunosurveillance
they are effectively eliminated. When mutated
cells escape immunosurveillance, a tumor and ma-
tegrated, and efficient cadre of defenses composed lignancy may develop.
of nonspecific mechanisms and a specific immune
system. Bellanti’ defines immunity as “. . . all of NONSPECIFIC IMMUNITY
those physiologic mechanisms that give man the Nonspecific defense mechanisms respond to any
capacity to recognize something as foreign to self entity recognized as ‘ ‘nonself’ ’ . The nonspecific
and to neutralize, eliminate, or metabolize it, with defense mechanisms to be discussed include phys-
or without injury to its own tissues.” Nonspecific ical and chemical barriers, inflammation, and
immunity includes innate barriers and responses to phagocytosis .
cellular injury and invasion that provide first-line
protection against potential pathogens. When the Physical and Chemical Barriers
first-line defenses are overcome, the specific im-
Physical barriers are the body’s first line of de-
mune system comes into play. The specific re-
fense against the external world.3 The skin is a
sponses are adaptive and acquired by exposure to
tough, resilient barrier that protects against micro-
invaders that are specifically recognized. There is
bial invasion both anatomically and chemically.
a great deal of collaboration and feedback between
As skin cells slough, so do bacteria. Pathogenic
nonspecific and specific immune defenses.
bacteria are prevented from colonizing on the skin
There are three major functions of the immune
because of the presence of normal flora. The skin’s
system: defense, homeostasis, and surveillance.’
low moisture content and antimicrobial substances
Defense, the function most readily attributed to
create an unfavorable environment for pathogenic
immunity, is protection against invasion by micro-
organisms. Minute breaks that occur regularly al-
organisms, ie, viruses, fungi, bacteria, and para-
low only small numbers of organisms that are usu-
sites. Sometimes the immune system malfunctions
ally controlled by other nonspecific defense mech-
and becomes hyperactive against things that would
anisms. Larger breaks due to trauma, bums, or
not ordinarily be harmful. This hyperactivity is
invasive procedures create a more hazardous situ-
manifested clinically as hypersensitivity and is the
ation.
pathophysiologic basis of immune disorders and
Mucous membranes of the respiratory and gas-
allergies. On the other hand, a hypoactive defense
trointestinal (GI) tracts act as physical barriers
leaves the host susceptible to infection.
against organisms that are inhaled or ingested. The
Homeostasis is a state of equilibrium of cells
ciliated epithelium of the upper airways and the
and internal processes. The immune system re-
trachea, hairs at the nasal openings, nasal secre-
moves damaged cells that result from normal ca-
tions, and the mechanical reflexes of bronchocon-
tabolism, growth, and injury. When a hyperactive
striction, coughing, and sneezing all help deny en-
immune system attacks cells that are not damaged,
try of microorganisms. Respiratory secretions
and thus not an appropriate target for this diligent
contain mucous, which serves as a trapping mech-
“cleanup crew’ ’ , an autoimmune disease results.
anism, secretory IgA, which neutralizes microor-
Surveillance is a process whereby immune cells
ganisms, and lysozymes, lactoferrin, and
recognize and remove mutant cells from the host.
a-1-antitrypsin, which are bactericidal.3 The GI
It is probable that mutant cells arise at a rate of 100
tract contains mucus and secretions that trap mi-
croorganisms. Gastric secretions are acidic and de-
stroy most ingested bacteria. Normal intestinal
From the National Institutes of Health, Bethesda, MD. flora, peristalsis, and rapid epithelial shedding and
Address reprint requests to Christine Grady, RN, MSN, CS,
3012 43rd St, Washington, DC 20016. evacuation inhibit the growth of pathogenic micro-
0 1988 by Grune & Stratton, Inc. organisms. Mucous membranes in the vagina, vag-
0749-2081188/0402-0001$05.00/0 inal secretions, the vaginal pH, and the presence of

86 Seminars in Oncology Nursing, Vol 4, No 2 (May), 1999: pp 96-94

HOST DEFENSE MECHANISMS: AN OVERVIEW
normal flora control the growth of microorganisms
there. Other physical barriers include the eyelids,
eyelashes, and lacrimal secretions that wash and
lubricate the eye surface.
Chemical barriers include acidic gastric secre-
tions, acid urine, the digestive enzymes
(lysozymes), and other antimicrobial substances in
nasal secretions, saliva, tears, breast milk, and se-
baceous and sweat secretions.
Inflammation
Inflammation is an immediate, aggressive re-
sponse by the body to physical injury (trauma,
bums, frostbite, etc) or bacterial invasion.4 In-
flammation is a series of cellular and systemic
events that occur in an attempt to restore or main-
tain homeostasis. Immediately after cell damage,
vessels contract and fibrin-plug formation begins.
Simultaneously, the vessels constrict for approxi-
mately 5 to 10 minutes. The vessel wall becomes
lined with leukocytes, erythrocytes, and platelets.
After the brief period of vasoconstriction, vasodi-
lation occurs and blood flow to the area is in-
creased. This produces redness and heat at the site.
Capillary permeability is increased, allowing the
leakage of plasma and cells into the interstitial
space, resulting in edema. The vascular changes
are mediated by substances such as histamine re-
leased at the site of injury. Histamine is a powerful
short-acting substance that causes vasodilation and
increased permeability. Longer-acting substances,
which continue the inflammatory response, in-
clude bradykinin and the prostaglandins, such as
PGE-2.
The fluid, plasma proteins, and cells that leak
into the interstitial spaces are collectively known
as the inflammatory exudate. Although the inflam-
matory exudate causes swelling and pain resulting
in restricted function of the inflamed part, it also
has several very important functions at the site of
injury: (1) It dilutes toxins released by bacteria. (2)
It carries nutrients necessary for tissue repair. (3) It
carries defensive cells that phagocytize, destroy
bacteria, and clean up the debris.3
In response to inflammation, there is an out-
pouring of leukocytes from the bone marrow and
the marginal pool. This is seen clinically as a leu-
kocytosis. The WBC count may rise from a normal
of 5,000 to lO,OOO/pL up to as high as 3O,OOO/pL.
The defensive cells in the inflammatory exudate
87
have a critical role in response to injury. Two types
of leukocytes are involved: (1) the neutrophil, a
polymorphonuclear leukocyte also sometimes re-
ferred to as apoly, seg, or PMN; and (2) the mono-
cyte, a mononuclear leukocyte.4 Both are derived,
as all blood cells are, from the bone marrow stem
cell (Fig 1). Neutrophils are attracted to the site of
inflammation within minutes by chemotactic sub-
stances released from bacteria and cells. Once at
the site, the neutrophils line the walls of the cap-
illaries (margination or pavementing), and then
migrate out of the permeable vessel wall, a process
called diapedesis. Neutrophils predominate in the
first two or three days after injury, while other
chemotactic substances are released to recruit
monocytes. Both neutrophils and monocytes func-
tion at the site as phagocytes (Table 1).4.5
Phagocytosis
A phagocyte, upon encountering a nonself in-
vader, extends a pseudopod formed by its cell
membrane to surround the invader. The invader is
then enveloped in a vacuole, referred to as a pha-
gosome. Phagocytic granules that contain diges-
tive enzymes then fuse with the phagosome, cre-
ating a phagolysosome. The enzymes are released
and destroy the offending substance (Fig 2).
Phagocytes also remove injured cells from dam-
aged tissues. Phagocytosis is enhanced by a pro-
cess known as opsonization. Several humoral sub-
stances, known as opsonins, coat the invading
eorinophils
phagocyte
monocytr
Fig 1. Diierentirtion of cells from the bone marrow stem
Cdl.
88 CHRISTINE GRADY

Table 1. Stages of the inflammatory Response

Staae I stage II stage Ill

Vascular Phagocytosis by neutrophils Regeneration

Initial vasoconstriction Arrival of monocytes, and Scar formation
Vasodilation transformation into macrophages
Increased permeability Phagocytosis by macrophages
Hemostasis Migration of fibroblasts,
Platelet-plug formation endothelial cells and other
Activation of coagulation cells for tissue repair
mechanisms
Cellular
Chemotaxis of neutrophils
Infiltration of the area
by neutrophils
Other
Formation of inflammatory
exudate
Systemic leukocytosis
Initial chemotaxis of monocytes
Release of endogenous
pyrogen (IL-l)

Data from Jett and Lancaster,’ and Stotts.’

antigen and make it more susceptible to phagocy- known as interleukin-1 (IL- 1). It appears that IL- 1
tosis. Antibodies, complement proteins, stimulates both T- and B-lymphocytes and en-
lysozymes, and other serum factors act as hances their function. This is one example of an
opsonins .3 important link between nonspecific and specific
Monocytes/macrophages predominate at the site immune mechanisms. IL-l also acts as endoge-
after the second or third day. Monocytes transform nous pyrogen, inducing prostaglandin production
into macrophages (literally, big eaters) as they go that causes fever and interferes with bacterial, vi-
from the intravascular to the interstitial spaces. ral, and perhaps tumor-cell growth.6
Macrophages not only phagocytize bacteria and Monocytes and other leukocytes also produce
other cellular debris, but also remove spent and the cytokine a-interferon (EN-CY) in response to
dead neutrophils. Monocytes/macrophages have a viral stimulation. IFN-(r inhibits virus replication
number of important immune functions, several of and enhances antiproliferative activities. In this
which will be discussed later. way, it contributes to host defense against viral
The activated macrophage releases a cytokine infections and tumor growth.

pseudopod formation and extension

roward the antigen

~~lo~ure of the antigen.

formation of phagosome

fusion Of granules Iwhich contain

lysozymesl with the phagosome

release of granular ContentS

digestion of antigen

Fig 2. The process of phagocytosis.

HOST DEFENSE MECHANISMS: AN OVERVIEW
SPECIFIC IMMUNITY
The specific immune response is characterized
by two properties, specificity and memory, which
distinguish it from nonspecific responses. Speci-
ficity limits the response of an immune cell to that
antigen for which it was designated. During devel-
opment, lymphocytes acquire receptors for specif-
ic antigens that commit them to a single antigenic
specificity for their life span. Memory is the prop-
erty that allows lymphocytes to respond in an ac-
celerated and augmented manner to antigens that
they remember. Because of memory, second or
subsequent exposures to an antigen result in a
quicker, more efficient immune response. This is
the scientific basis for immunization.
Humoral and Cell-Mediated Immunity
There are two main types of effector mecha-
nisms that comprise specific immunity, humoral
immune mechanisms and cell-mediated immune
mechanisms. Each type involves different cells,
produces different products, and functions in a dif-
ferent way. However, there is considerable coop-
eration, interaction, and interdependence between
them (Fig 3).
Some knowledge of lymphocytes is helpful in
order to understand humoral and cell-mediated im-
munity. Just as phagocytic leukocytes are respon-
sible for phagocytosis in the nonspecific system,
T cell
Fig 9. Humoral
89
lymphocytes are responsible for specific immune
system responses. Lymphocytes normally make up
30% to 40% of the circulating pool of leukocytes.
Lymphocytes, the smallest leukocytes, are mono-
nuclear, and are derived from the bone marrow
stem ceI1 through the lymphoid lineage. There are
at least three types of lymphocytes; B-cells, T-
cells, and large granular lymphocytes
(LGL). 1,2,4,6,7
T-lymphocytes are responsible for cell-mediated
immunity (CMI). Approximately 80% of circulat-
ing lymphocytes are T-cells. The T-cell matures
and develops competence in the thymus gland (T,
thymocyte or thymus-derived lymphocyte), and
then migrates to the peripheral lymphoid tissues.
T-cells are further subdivided into subsets with dis-
tinct functions and surface proteins. One subsetis
the TCcell subset, so called because the cells have
a surface protein (T4- or CD4-molecule) recog-
nized by the OKT4 monoclonal antibody. TCcells
function as inducer- or helper-cells in CMI. An-
other subset is the TS-cell. T8-cells function as
cytotoxic and suppressor cells. Normally, T6cells
outnumber T&ells by approximately two-to-one.
The main functions of the T-lymphocytes and their
products, lymphokines, are induction of other im-
mune components, cytotoxicity, and immunoreg-
ulation. CMI protects the host against intracellular
organisms (viruses, fungi, parasites) and tumors,
and is responsible for immunosurveillance and
graft rejections.
0
prollferatlon
dtfferentiation
immunity Y cell-mediated immunity.

B-lymphocytes are responsible for humoral im-
munity. It is thought that the B-cell matures and
develops competence in the bone marrow, but this
has not been definitively established. B-cells have
different surface proteins than T-cells, including
immunoglobulin and receptors for C3b (a comple-
ment split product) and the Fc portion of immuno-
globulin. Mature B-cells are found along with T-
cells in peripheral lymphoid tissues and in the
peripheral circulation (12% to 15% of circulating
lymphocytes). Antibody is the product of B-cells
that mediate humoral immunity. Humoral immu-
nity protects the host against bacteria and viruses.
Large granuZar lymphocytes, also known as nat-
ural killer cells (NK cells), lack the markers of
either the T-cell or the B-cell. As the name NK cell
implies, their primary function is cytotoxicity. NK
cells destroy nonspecifically without prior sensiti-
zation, and they have no immunologic memory.2
The primary targets of NK cells are tumor cells and
virally infected cells.
Lymphoid Organs
Lymphocytes develop and mature in primary
lymphoid organs, and are stored and activated in
secondary lymphoid organs. The primary lym-
phoid organs include the bone marrow and the thy-
mus . Secondary lymphoid organs include lymphat-
ic vessels and lymph nodes, spleen, liver, and
patches of lymphoid tissue such as Peyer’s patches
in the intestine. Lymphatic vessels are a network
of small vessels that merge into increasingly larger
vessels, and transport lymph and lymphocytes. All
the lymphatics except those which feed the right
head, neck, and thorax, eventually empty into the
thoracic duct. The thoracic duct and the right lym-
phatic duct empty into the large veins of the vas-
cular system. Lymph nodes are small, bean-shaped
structures found at the junction of lymphatic chan-
nels. Lymph nodes are a storage place for T-cells,
B-cells, and macrophages. The endothelium of the
vein in the lymph node (postcapillary venule) is
continuous with the endothelium of the lymphat-
its. This allows lymph to exit the venous circula-
tion, filter through and be replenished in the lymph
node, and exit through the efferent lymphatics
back into the lymphatic system. Lymph is eventu-
ally transported back into the vascular system
through the tboracic duct. A vitally important cir-
culating pool of lymphocytes is thus made avail-
able to act in any part of the body.
CHRISTINE GRADY
Specific Immune Response
The immune response can be broken down into
two phases or limbs. The afferent limb involves the
phases of recognition of antigen by the lympho-
cyte, and subsequent activation, proliferation, and
differentiation of the lymphocyte into an effector
cell.’ The efferent limb involves the effector func-
tions performed by fully differentiated lympho-
cytes and their products. Since the purpose of the
immune system is to prevent harm to the host,
microorganisms, mutated cells, and damaged cells
are recognized during the afferent limb and the
mechanisms are set into motion so that harm is
eliminated or minimized during the efferent limb.
AfSerent Limb: Recognition and Activation
Recognition of antigen by lymphocytes is a well
controlled and complex event, regulated by im-
mune-response genes that are part of the major
histocompatibility complex (MHC), also known as
the human-leukocyte-antigen (HLA) genes, lo-
cated on the sixth chromosome.1S2V5 The HLA
genes code for histocompatibility antigens that ap-
pear on the surface of all nucleated cells. The HLA
genes are divided into specific regions, or loci,
designated as HLA-A, HLA-B, HLA-C, HLA-D,
and HLA-DR. These are divided into two classes.
Class I genes include the HLA-A, -B, and -C re-
gions, and are the classic histocompatibility anti-
gens present on all cells. Class II genes code for
HLA-D and -DR antigens, which are found on the
surface of macrophages and B-cells. The DR gene,
known as the immune-response gene, has a direct
effect on the ability of an individual to respond to
an antigen.6
Recognition and activation of a T4-cell takes
place as follows: An antigen is picked up by a
macrophage, processed, and presented to the T4-
cell. The macrophages also release a cytokine, IL-
1. The T4-cell has surface receptors that recognize
and bind to the presented antigen and to the class II
DR molecule on the surface of the macrophage.
Binding with these two molecules plus stimulation
by IL- 1 from the activated macrophage activate the
T4-cell. Without the associated recognition of the
self DR molecule on the macrophage, activation of
the TCcell will not occur. This is known as the
MHC restriction. ’ Y276*8 The activated T4-cell pro-
liferates rapidly to produce many similar cells, and
begins to produce lymphokines. Lymphokines
HOST DEFENSE MECHANISMS: AN OVERVIEW
send powerful signals to other cells of the immune
system. An important lymphokine produced by the
activated T6cell that enhances TCcell prolifera-
tion and differentiation is interleukin-2 (IL-2). Ac-
tivated T4-cells also develop IL-2 receptors that
bind to the generated IL-2, resulting in enhance-
ment of the proliferation and differentiation (Fig 4,
top) ,6,*
Recognition and activation of T8-cells is also
quite specific. The cytotoxic T8-cell recognizes
foreign or altered class I MHC molecules on cell
surfaces. For example, a tissue graft that had a
foreign class I MHC molecule, or a cell in which
the class I molecule had been altered by a viral
infection or mutation, might be recognized by a
T8-cell, The T8-cell binds to the class I MHC mol-
ecule via receptors on its surface, and then begins
to generate IL-2 receptors, The IL-2 released by
the activated T4-cell then binds with the newly
generated IL-2 receptors on the T8-cell, and pro-
liferation begins.7 It appears that T8-cells need the
induction signal (IL-2) from the T4-cell in order to
proliferate and function (Fig 4, middle).
I IL-2
self DR
Fig 4. Recognition of antigen.
91
The B-cell usually becomes activated by recog-
nizing and binding to partially exposed antigen on
the surface of the macrophage that is already
bound to the T4-cell. At the same time, receptors
on the T4-cell bind to the HLA-DR molecules on
the B-cell surface. This tricellular compiex acti-
vates the B-cell which then generates receptors for
B-cell growth factor (BCGF).678 BCGF, a lym-
phokine released by the activated TCcell, binds to
the receptors, and the B-cell proliferates. Some of
the new B-cells then generate receptors for another
T4-cell lymphokine, B-cell differentiation factor
(BCDF). B-cells bind BCDF and differentiate into
plasma cells which synthesize and secrete immu-
noglobulin or antibody (Fig 4, bottom).
It is apparent that activation of lymphocytes is a
process that necessitates sequential cooperation
among several different cells. The macrophage is
the major antigen-presenting cell and the source of
IL-l. The T4-cell is the inducer cell and the source
of IL-2. The T8-cell and the B-cell are then acti-
vated in a specific manner and proliferate to form
a clone of defensive cells.
Efferent Limb
The efferent limb is the response phase, in
which the real defensive work is accomplished.
The processes described thus far prepare the way
for the effector functions of specific immunity. Ef-
fector functions include antibody production, lym-
phokine release, cytotoxicity, and immunoregula-
tion .
Antibody. Antibody is an immunoglobulin
synthesized by the plasma cell, the final cell of
B-cell differentiation. The immunoglobulin mole-
cule is composed of four chains of amino acids
held together by disulfide bonds.‘*234Y6-8One end
of the immunoglobulin molecule, termed Fub for
antigen-binding fragment, has a highly variable se-
quence of amino acids specific to the antigen for
which it was formed. The other end of the mole-
cule, the Fc, or constant fragment, has a sequence
of amino acids that remains constant within a given
class of antibody. In humans, there are five classes
of antibody: IgG, IgA, IgM, IgE, and IgD (Table
2v4v6-8 An antibody binds with the antigen for
which it was made by combining at the Fab portion
of the molecule. This complex of antigen and an-
tibody is referred to as an immune complex. An-
tibody participates in many different ways to elim-
92 CHRISTINE GRADY

Table 2. Human lmmunoglobulins

Serum Concentration
lmmunoglobulin and Location Activih/ Other

75% in serum; Opsonization Crosses placenta

intravascular, Neutralization Secondary response ab
extravascular Complement fixation
17% in serum; Neutralization Found in breast
also found in Prevention of milk
mucous membranes surface attachment
and secretions
7% in serum; Agglutination Primary antibody,
intravascular Complement fixation natural blood
group AB
bE 0.1% in serum; Release of histamine Involved in
bound to cells and other mediators type I hyper-
(mast cells and from mast cells sensitivity
basophils) “reaginic antibody” reactions
W Nondetectable in serum Unknown May function as a
Surface of B-ceils receptor on the
B-cell surface

inate antigen and defend the body. Some some are anaphylatoxins (agents that increase va-
antibodies neutralize the antigen, ie, render it sodilation and capillary permeability). All enhance
harmless by interfering with its ability to attach to phagocytosis.
cells and set up infection. Other antibodies act as Thus an antibody, produced by a fully differen-
opsonins, coating the antigen to facilitate phago- tiated B-cell of the humoral line of immunity,
cytosis. Still other antibodies form complexes that binds to the antigen that induced its formation, and
are removed by precipitation or agglutination. Cer- binds to another cell or substance (phagocyte, Fc-
tain immune complexes are eliminated by cells that
have Fc receptors and function cytotoxically. This
is called antibody-dependent cellular cytotoxicity
(ADCC). Sometimes antibodies work to eliminate
antigen by fixing complement, resulting in com-
plement-mediated lysis. ‘-476-8
Complement is the name given to a group of
circulating proteins labeled Cl through C9, inclu-
sive. When the first component of complement be-
comes activated by an immune complex containing
IgG or IgM, it sets off a series of biochemical steps
whereby, in a cascade fashion, each complement
component becomes activated. This is called the
classical pathway of complement activation (Fig
5). The ultimate goal of complement activation is
the destruction of the target by lysis. Lysis is ac-
complished by the C5 to C9 unit, termed the mem-
brane-attack component, which literally pokes a
hole in the target cell membrane, allowing its con-
tents to leak out and the target cell to die. Besides
cell lysis, the split products of complement activa-
tion function in other important ways to augment
immune function. Some complement split-
products are chemotaxins, others are opsonins , and Fig 5. Complement cascade.
HOST DEFENSE MECHANISMS: AN OVERVIEW 93

receptor cell, complement) that will carry out the Induces T8 cells to suPPreSS

antigen’s destruction. 1-4*6-9

Induces B cells to Induces phagocytes
Lymphokine release. Lymphokines produced make antibody to phagocytose
by the T4-cell include those which (1) enhance/
induce phagocytosis, such as macrophage chemo-
Induces T8 cell
tactic factor (MCF), macrophage migration- to kill 0 T4 cell

inhibition factor (MIF), macrophage activation

factor (MAF), leukocyte chemotactic factor
(LCF), and others; (2) induce T-cell growth, dif-
ferentiation, and function, such as IL-2, and
y-interferon; (3) induce B-cell growth and func-
tions, such as BCGF and BCDF; (4) enhance cy-
totoxicity, such as y-interferon and IL-2; and (5)
include others, such as colony stimulating factor
(CSF), which induces the growth and differentia-
tion of monocytes; and tumor necrosis factor
(TNF), formerly called lymphotoxin, which de-
stroys tumor cells (Table 3).2q6,9
Lymphokines induce T4-cells to grow and dif-
ferentiate, some TS-cells to be cytotoxic, other T8-
cells to suppress, B-cells to produce antibody, NK
cells to kill, and macrophages and other phago-
cytes to phagocytose. The T4-inducer cell is often
referred to as the conductor of the immune orches-
tra because, without its direction, all immune func-
tions are abnormal, and the symphony does not get
played (Fig 6).
Cyrotoxicity. Cytotoxicity or the killing of tar-
get cells is accomplished by three major mecha-
nisms:
(1) The NK cell nonspecifically targets tumor
cells and virally infected cells and destroys them.
The exact mechanism of NK cell-mediated de-
struction is not known. NK function is augmented
by the lymphokines -y-interferon and IL-2, by the
cytokine a-interferon, and by certain bacterial
adjuvants.296Y899
Table
Induces NK cell Induces B cells to
to kill grow and function
*
Induces T cells to
grow and funcrion
Fig 6. T4-lymphocyte-inducer function.
(2) T8-cell cytotoxicity is specific and targeted.
There is recognition of and binding with nonself or
altered-self class I HLA molecules, resulting in
activation, as described above. The recognition
process, coupled with inducement by the T4 lym-
phokine IL-2, results in a clone of T8-cells that
cytotoxically destroy the target cell. 2,6,8
(3) ADCC, described earlier, is a process by
which a cell with an Fc receptor binds to the Fc
portion of an immunoglobulin that is bound to an-
tigen. The cell with the Fc receptor is capable of
destroying the antigen and actually eliminating the
immune complex. *z6 ADCC is indirectly depen-
dent on Tbcell induction because of the coopera-
tion that occurs to induce B-cell to make antibody.
Zmmunoregulation. T-cells play a crucial role
in regulating immune responses.1-3,6 The T4 sub-
set of lymphocytes release substances that help the
B-cell differentiate into antibody-producing
plasma cells that make antibody. The T8 subset of
lymphocytes is capable of inhibiting and suppress-
ing B-cell differentiation and antibody production.
T4 inducers and T8 suppressors also have a role in
regulating other aspects of the immune response.
3. Lymphokines

Lymphokine Function

Macrophage-chemotactic factor (MCF) Enhance phagocytosis

Macrophage-inhibition factor (MIF)
Macrophage activation factor (MAF)
Leukocyte-chemotactic factor (LCF)
Interleukin-2 (IL-2) Enhance T-cell growth and function
B-cell growth factor (BCGF) Enhance B-cell growth and function
B-cell differentiation factor (BCDF)
Gamma Interferon (yIFN) Enhance cytotoxicity
Interleukin-2 (IL-2)
Colony-stimulating factor (CSF) Enhance growth and differentiation of monocytes
Tumor necrosis factor (TNF) Enhance destruction of tumor cells
94
Immunoregulation is a very complex process that
is still only partially understood.
Memory
Both T- and B-lymphocytes appear to have im-
munologic memory. When T-cells or B-cells are
activated in response to a specific antigen, they
proliferate and differentiate into effector cells and
memory cells. Memory cells remain in the host
prepared and awaiting a subsequent exposure to
the same antigen. Upon repeated exposure, the
memory lymphocyte responds more quickly and in
a more augmented fashion than that which oc-
curred on the primary exposure. The response by
REFERENCES
1. Bellanti J: Immunology, Basic Processes. Philadelphia,
Saunders, 1985
2. Roitt I, Broff J, Male D: Immunology. St Louis, Mosby,
1985
3. Fauci A: Host-defense mechanisms against infection:
Current concepts. Upjohn Company, 1979
4. Jett M, Lancaster L: The inflammatory-immune response:
The body’s defense against invasion. Crit Care Nurse 3: Sept/
Ott, 1983
5. Stotts N: Impaired wound healing, in Garrieri V, Lindsey
CHRISTINE GRADY
memory cells to antigen is called the secondary or
anamnestic response.
SUMMARY
It is clear that the immune system, or host de-
fense system, is a multifaceted system of unique,
yet highly integrated, responses to potentially
harmful antigens or mutated cells. Nonspecific de-
fenses provide the first line of protection. Specific
defenses, in the form of humoral (B-cell) immuni-
ty and cell-mediated (T-cell) immunity provide the
sophisticated mechanisms that help keep us free
from infection, malignancy, and autoimmune dis-
eases.
A, West C (eds): Pathophysiological Phenomena in Nursing.
Philadelphia, Saunders, 1986
6. Stites D, Stobo J, Funderberg H, et al: Basic and Clinical
Immunology (ed 6). Los Altos, CA, Lange, 1987
7. Gurevich I: The competent internal immune system. Nurs
Ciin North Am 20:151-160, 1985
8. Cronenberger H: Nonimmune and immune defenses: A
review. J Med Tech 2:701-708, 1985
9. Smith S: Physiology of the immune system. Crit Care
Quart 9:45-49, 1986