JOG” PRINCIPLES & PRACTICE
Immunologic Adap tations
During Pregnancy
Kristen D . Priddy, RNC, MSN, CNS
= Many complementarychanges occur in a preg-
nant woman’s immune system to protect the fetus
from attack while maintaining maternal defenses
against disease. Enhancements occur in immune el-
ements that fight bacterial infections. Conversely,
suppression of T-cell activity causes increased sus-
ceptibility to viral infections, such as hepatitis, ru-
bella, herpes, and human papillomavirus, and leads
to an irreversible reduction in helper T cells in women
infected with the human immunodeficiency virus. Lo-
cal secretion of corticosteroids and changes in cyto-
kine concentration in the reproductive tract protect
the fetus from rejection. Understanding these changes
assists the perinatal nurse in assessing and counsel-
ing women of childbearing age. IOGNN, 26,388-
394; 1997.
Accepted: May 1996
Pregnancy is a normal, healthy state for most
women. Why, then, do some mild infectious agents
lead to profound illness during pregnancy, whereas
others do not? Why do some conditions improve
during pregnancy, whereas others worsen? Why
are genital tract infections so frequent during preg-
nancy? What impact do maternal immune changes
have on immune-mediated diseases, such as infec-
tion with human immunodeficiency virus (HIV),
systemic lupus erythematosus, and rheumatoid ar-
thritis? And how, with a healthy immune system,
can a woman’s body tolerate the presence of a for-
eign chromosome set in the fetus?
Pregnancy requires physiologic adaptations
in all maternal systems, including the immune sys-
tem. Knowledge about the immune system has
grown during the past few decades, with many re-
searchers focusing on the immunologic adapta-
tions of pregnancy. Most researchers have ap-
388 IOGNN
proached the issue of immune changes during preg-
nancy by likening the fetus to a transplanted organ,
raising the question of how pregnancy is tolerated
by the maternal immune system and carried to
term without graft rejection. The term allogenic
graft refers to transplanted tissue from an organism
within the same species that is not a chromoso-
mally identical twin. From the perspective of trans-
plant immunology, the fetus is a semiallogenic
graft, which means that the “host” (the mother)
recognizes the fetus as half foreign and half self
(Head & Billingham, 1982). Thus, it might appear
that pregnancy must be an immunosuppressed
state, because deliberate immunosuppression is the
only means known for preventing graft rejection.
Enhancement and suppression of
different immune mechanisms create a
balance that protects the fetus without
compromising the mother.
Other researchers believe that it would not
make biologic sense to compromise the mother’s
immune system when protection of the fetus is cru-
cial (Branch & Scott, 1994; Daunter, 1992). Fur-
ther, the concept of significant immunosuppression
during pregnancy has not been borne out clinically.
What becomes apparent is a balance in pregnancy
between enhancement of certain immune mecha-
nisms and suppression of others.
Nursing care of the woman of childbearing
Volume 26, Number 4
 age requires an understanding of the pregnancy-induced
changes in immune response. In this article, a brief ex-
planation of normal immune mechanisms and a review
of immune adaptations during pregnancy are provided.
Human Immunity
Human immunity is a system of interacting re-
sponses that can be divided into nonspecific and specific
mechanisms (Guyton, 1991). Nonspecific responses,
sometimes called innate immunity, are the general pro-
cesses by which the body resists infection (Guyton,
1991). Specific immunity, also called acquired immunity,
refers to mechanisms directed at specific infectious
agents (see Table 1).
Nonspecific lmmune Mechanisms
Nonspecific immune mechanisms include phago-
cytosis, the complement system, natural killer cells, and
cytokines, as well as the mechanical barrier to bacteria
provided by intact skin and mucous membranes (Lar-
occo, 1994).
Phagocytosis. Phagocytosis is the process by which
bacteria are ingested and destroyed. Phagocytosis occurs
in four stages, using two types of white blood cells. These
are the neutrophils or polymorphonuclear leukocytes
(PMNs), so named because of their multilobed nuclei,
and the macrophages. The first stage of phagocytosis is
called chemotaxis. White blood cells move to sites of
bacterial infection. Polymorphonuclear leukocytes are
the first to arrive on the scene, usually within 90 minutes
of injury. The larger monocytes, also called macro-
phages, arrive later, usually within 48 hours, and ingest
larger quantities of bacteria and debris than the PMNs.
The second phase of phagocytosis, opsonization, occurs
as invading cells are made more susceptible to ingestion.
Immunoglobulin IgG and the C3b fragment of the com-
plement system are examples of opsonins. In the third
stage, phagocytes recognize the agents as foreign and en-
gulf them. In the final stage of phagocytosis, ingested
particles are digested by proteolytic enzymes and lipases
or killed by bactericidal substances, such as oxidizing
agents (Guyton, 1991; Larocco, 1994).
Nonspecific immunity is enhanced during preg-
nancy. The number of white blood cells is increased and
their function is improved. White blood cell count nor-

TABLE 1
Components of Immune Response

Nonspecific (innate) immunity
Specific (acquired) immunity
Humoral immunity
Cell-mediated immunity
Polymorphonuclear leukocytes and Engulf and kill invading bacteria
macrophages
Natural killer (NK) cells Kill tumor cells and virus-infected host
cells
Complement system Produces lytic complexes which destroy
infecting agents
Cytokines (i.e., interleukins, Hormone-like polypeptides produced
interferons, tumor necrosis factor, by white blood cells, which serve
colony-stimulating factor) several functions, including fever
induction, stimulation of T and B cells,
and destruction of tumor cells
B cells Recognize antigens and synthesize
antibodies; mediate allergic response;
kill bacteria; eliminate bacterial toxins;
and prevent reinfection by viruses
Antibodies (i.e., immunoglobulin Bind to foreign cells, allowing
(Ig)A, IgD, IgE, I&, and IgM) recognition by NK cells and T cells
T cells Stimulate T and B cells; control viral
infections; reject grafts; cause delayed
hypersensitivity reactions; secrete
cytokines
Helper T cells Stimulate antibody production; increase
cytotoxicity of killer T cells
Suppressor T cells Inhibit B cell Ig secretion and
cytotoxicity of killer T cells
Killer T cells Destroy invading cells with antibody
markers

JulylAugust 1997 JOG" 389

 mally increases from the nonpregnant norm of 5,000-
10,000/mm3 (Ravel, 1995)to a range of 6,000-12,000/
mm3, with the greatest increase in numbers of circulating
PMNs (Blackburn & Loper,-1992;Branch & Scott,
1994). Barriga, Rodriguez, and Ortega (1994)found
that attachment, ingestion, and digestion of Candida al-
bicans by PMNs from the blood of normal pregnant
women was enhanced. They suggest that the “stimula-
tory effect of human chorionic gonadotropin on circu-
lating [PMNs]” may be responsible for this enhancement
(p. 45). However, yeast infections occur in approxi-
mately 15% of pregnant women, possibly because in-
creased estrogen levels in the reproductive tract lead to
higher concentrations of nutrients that support fungal
growth (Gibbs & Sweet, 1994).Shibuya, Isuchi, and Ku-
roiwa (1991)also note enhanced antibody expression on
PMNs of pregnant women, leading to readier recog-
nition of antigen-antibody complexes and improved
phagocytosis.
Conversely, phagocytic activity is decreased
around the fetus and placenta because of increased local
concentrations of corticosteroids in the reproductive
tract (Branch & Scott, 1994).Some authors have re-
ported reduced phagocytic activity, especially in re-
sponse to gram-negative organisms (Blackburn & Loper,
1992).This may explain why pregnant women are more
likely to experience disseminated gonococcal infection
when exposed to the gram-negative bacteria Neisseriu
gonorrhoeue. Disseminated gonococcal infection is char-
acterized by an early bacteremic phase, with chills, fever,
and skin lesions, which progresses to a second, septic
arthritic stage (Gibbs & Sweet, 1994).This reduced abil-
ity during pregnancy to resist growth of gram-negative
bacteria explains the ability of N. gonorrhoeue to invade
the uterus and increase the incidence of premature rup-
ture of membranes, prematurity, intrauterine growth re-
tardation, neonatal sepsis, and postpartum endometritis
(Gibbs & Sweet, 1994).In addition, maternal response
to infection may be delayed by the slower chemotaxis of
pregnancy (Blackburn & Loper, 1992).Because of local
hormonal changes in the reproductive tract that seem to
encourage bacterial growth, screening for gonorrhea and
other sexually transmitted diseases and vaginal infec-
tions should be a routine part of the initial prenatal visit.
The perinatal nurse can educate the patient on the in-
creased risks of intrauterine growth retardation, pre-
mature rupture of membranes, and infection and the im-
portance of adhering to recommended treatment and
prevention regimens.
The Complement System. The complement system
is a protein cascade that culminates in the synthesis of
powerful lytic complexes for the destruction of infectious
agents. Much like the clotting cascade, the complement
proteins circulate in the bloodstream until needed. The
complement system may be triggered via the classical
390 JOG”
pathway, when IgG or IgM antibodies bind to a foreign
antigen, or via the alternative pathway, when it responds
directly to substances on the surfaces of invading cells
(Alberts et al., 1983).
Beginning at 11 weeks of gestation, maternal se-
rum complement elevations occur that enhance chemo-
taxis and Ig opsonization to improve maternal defense
against bacterial invasion (Blackburn & Loper, 1992).
Some proteins involved in the activation of the classical
and the alternative pathways are decreased, possibly de-
laying involvement of the complement system in immune
response. Blackburn and Loper (1992)suggest that this
delay may assist in protecting the fetus and trophoblast
from attack by the maternal immune system.
Systemic lupus erythematosus is a disease in which
autoimmune complexes cause tissue damage in several
systems, including the joints and kidneys. Lupus flares
occur three times more frequently in women who are
pregnant than in women who are not pregnant (Mabie,
1991).Lupus antibodies during pregnancy are associ-
ated with increased congenital heart block and increased
risk of thrombosis, intrauterine growth retardation, re-
current spontaneous abortion, and stillbirth (Mabie,
1991).Reduction of suppressor T-cell function during
pregnancy allows B cells to more readily form antibody-
antigen complexes (Blackburn & Loper, 1992).Active
systemic lupus erythematosus immune complexes con-
sume serum complement and may lead to lower levels of
complement. Because complement normally is elevated
during pregnancy, it is important to evaluate the change
in complement level over the course of the pregnancy
(Mabie, 1991).
Natural Killer Cells. Natural killer (NK) cells are
circulating large white blood cells that can kill tumor
cells or virus-infected host cells with or without antibody
markers. Natural killer cell activity is enhanced by the
cytokine interleukin-2 (IL-2) (Larocco, 1994).
Actual numbers of circulating NK cells may remain
at normal levels or decrease only slightly during preg-
nancy (Branch & Scott, 1994).Increased levels of pros-
taglandin E2 in the uterus inhibit NK activity (Daunter,
1992;Wood, 1994).Alterations in the production of IL-
2 also may result in decreased NK activity (Wegmann,
Lin, Guilbert, & Mosmann, 1993).To protect the fetus
from attack by the maternal immune system, the tro-
phoblast presents minimal expression of the antigen ma-
jor histocompatibility on its surface (Lederman, 1984;
Wegmann et al., 1993;Wood, 1994).However, because
NK cells can respond to foreign cells without benefit of
antigen recognition, they have the potential to damage
the conceptus. Mice are more likely to resorb their fe-
tuses if NK activity is not suppressed by their placentas
(Wegmann et al., 1993).This indicates that suppression
of NK cells may be necessary for protection of the fetus
and trophoblast but may inhibit maternal resistance to
Volume 26, Number 4
 TABLE 2
Clinical Manifestations of Immune Changes During Pregnancy
ClinicaiManifestation
Frequent yeast infections
Increased risk of disseminated
gonococcal infection
Asymptomatic bacteriuria that is due to
E. coli
Decreased resistance to intracellular
pathogens (e.g., Listeria and
Toxoplasm)
Group B streptococcus
Flares of systemic lupus erythematosus
Remission of rheumatoid arthritis
Increased risk of contracting viral illness;
more fulminant course of viral illness
Permanent reduction of CD4 (Helper T-
cell) count in women who are HIV
positive
False-negativetuberculosis test
intracellular pathogens such as Listeria and Toxoplasma
(Wegmann et al., 1993).
Cytokines. Cytokines are hormone-like polypep-
tides produced primarily by lymphocytes and macro-
phages during the early phases of the immune response.
These substances serve several immune functions, in-
cluding induction of fever; activation, differentiation,
and growth of T and B lymphocytes; stimulation of an-
tigen expression; and direct cytotoxicity to tumor cells.
Cytokines include IL 1-8, alpha and beta interferon, tu-
mor necrosis factor, and several colony-stimulating
factors.
As in the complement system, relative increases
and decreases in specific cytokines during pregnancy de-
pend on the functions of those cytokines. Cytokines may
play a role in the premature rupture of membranes in
the presence of chorioamnionitis by stimulating produc-
tion of proteolytic enzymes in maternal phagocytes that
break down fetal membranes (Blackburn & Loper,
1992). Lederman (1984)notes that “maternal serum can
also block the secretion of the lymphokine macrophage
inhibitory factor,” a cytokine responsible for sequester-
ing macrophages in areas of perceived foreign invasion,
such as the uterus (p. 7s).Two types of lymphocytes, T-
Helper 1 (TH1) and T-Helper 2 (TH2) secrete two
groups of cytokines that serve to regulate one another
(Banchereau & Miossec, 1993). Wegmann et al. (1993)
speculate that the conceptus may secrete T H 2 cytokines.
julylAugust 1997
Underlying Immunologic Change
Increased estrogens in reproductive tract
Increased corticosteroids in
reproductive tract; decreased
phagocytosis of gram-negative
organisms
Decreased phagocytic activity
Suppression of natural killer cells
Reduced immunoglobulin
Increased B-cell activity
Suppressed T-cell function
Suppressed T-cell function
Suppressed T-cell function
Suppressed T-cell function
This local secretion of cytokines in the reproductive
tract, including granulocyte-macrophage colony-stimu-
lating factor, colony-stimulating factor-1, and IL-3, has
been shown to promote growth of the trophoblast and
enhance fetal survival. T-Helper 2 cytokines also down-
regulate or reduce TH1 cytokines known to be harmful
to the fetus and trophoblast, including IL-2, interferon
gamma, and tumor necrosis factor. As mentioned above,
IL-2 stimulates the activity of NK cells, which can dam-
age the trophoblast and fetus. Tumor necrosis factor
would logically attack a fetus perceived by the body as
a tumor. Local secretion of the growth-enhancing cyto-
kines in the reproductive tract alters the equilibrium be-
tween the TH1 and TH2 cytokines, protecting the fetus
without significantly compromising maternal immune
response (Wegmann et al., 1993). Table 2 lists immune
changes during pregnancy.
Specific Immune Mechanisms
Specific immune mechanisms include responses ac-
quired after exposure to specific antigens (Guyton,
1991). These responses are divided into humoral im-
munity and cell-mediated immunity.
Humoral Immunity. Humoral immunity is medi-
ated by B-lymphocytes, whose primary purpose is to rec-
ognize antigens and synthesize antibodies. The antibod-
ies bind to the foreign cells, enabling NK cells, effector
T cells, and complement to identify and destroy them
JOGNN 391
 (Alberts et al., 1983). In this way, humoral immunity
mediates several responses, including immediate allergic
response, killing of invading bacteria, elimination of bac-
terial toxins, and prevention of reinfection by viruses
(Larocco, 1994). The antibodies produced are called im-
munoglobulins (Ig) and are subdivided into IgA, IgD,
IgE, IgG, and IgM. Immunoglobulin G and M are pri-
marily responsible for defense against invading bacteria,
and each stimulates the complement system (Alberts et
al., 1983). Immunoglobulin G, the only Ig that crosses
the placenta, is responsible for passive immunity during
the neonatal period (Alberts et a]., 1983; Blackburn &
Loper, 1992). Immunoglobulin A is the Ig found in the
largest quantity in secretions and is present in human
breast milk, with many other immunologic factors
(Blackburn & Loper, 1992). Immunoglobulin E medi-
ates allergic responses. Immunoglobulin D is rarely syn-
thesized, and its functions are unknown.
Although most Igs remain stable during pregnancy,
some researchers have reported reductions of 15% to
32% in IgG (Blackburn & Loper, 1992). These reduc-
tions may be due to hernodilution, spilling of IgG in
urine, or transfer of IgG across the placenta during the
last trimester and may lead to increased risk of strepto-
coccal colonization (Blackburn & Loper, 1992).
Wegmann et al. (1993) suggest that fetal secretion
of cytokines “redirects maternal immunity away from
cell-mediated immunity toward enhanced humoral re-
sponsiveness” (p. 353).They cite increased B-cell activity
shown by greater incidence of flare-ups of systemic lupus
erythematosus during pregnancy. They also note that
pregnant mice exhibit enhanced B-cell response when in-
jected with red blood cells from sheep. Intact or en-
hanced humoral response may help compensate for ad-
justments in other immune mechanisms through a more
aggressive attack on invading bacteria. In addition, an
intact humoral system may be necessary for the secretion
of blocking antibodies that protect the fetus from attack
by maternal T cells (Blackburn & Loper, 1992).
Cell-Mediated Immunity. T cells are the lympho-
cytes that function in cell-mediated immunity. T cells
stimulate other T and B cells, control viral infections,
reject grafts, and mediate delayed hypersensitivity reac-
tions (Larocco, 1994). The three types of T cells are
helper T cells, suppressor T cells, and cytotoxic or killer
T cells. Helper T cells, also called CD-4 cells, stimulate
antibody production and increase cytotoxicity of killer
T cells. Suppressor T cells, as their name suggests, sup-
press immune response by inhibiting Ig secretion of B
cells and cytotoxicity of killer T cells. Killer T cells de-
stroy invading cells that have been marked by antibod-
ies. All T cells secrete cytokines.
Because one of the primary responses of T cells is
graft rejection, cell-mediated immunity poses the great-
est threat to the fetus. Not surprisingly, many investi-
392 JOGNN
gators have found decreases in T-cell function in preg-
nant women. Nakamura et al. (1993) observed a sup-
pression of Epstein-Barr-virus-specific cytotoxic T cells
during pregnancy, with the greatest reduction occurring
during the 1st trimester. Normal T-cell response re-
turned at 1 month postpartum. Mentlein, Staves, Rix-
Matzen, and Tinneberg (1991) found reduced numbers
of T cells and a lower capacity of T cells to secrete IL-2
and proliferate in response to antigen stimulation. Led-
erman (1984)also notes that the ability of maternal lym-
phocytes to proliferate in response to either soluble an-
tigens or foreign lymphocytes is diminished during the
2nd and 3rd trimesters of pregnancy, as is the ability of
T lymphocytes to kill foreign cells. Pregnancy-associated
glycoproteins found in maternal serum also inhibit T-
cell proliferation, as do fetal lymphocytes (Lederman,
1984). Wegmann et al. (1993)cite as further evidence of
T-cell suppression the remission of rheumatoid arthritis,
a cell-mediated autoimmune disorder, experienced by
70% of pregnant women who have arthritis. Some re-
searchers have shown that although absolute numbers of
T cells do not decrease during pregnancy, the ratio of
helper and suppressor T cells changes, resulting in sup-
pression of T-cell function (Blackburn & Loper, 1992;
Branch & Scott, 1994; Lederman, 1984). This reduction
in absolute numbers of T cells and change in the ratio of
helper T cells to suppressor T cells is similar to the
changes that occur in people with HIV. Immunologic
function in people with HIV is evaluated through labo-
ratory CD4 (helper T-cell) and CD8 (suppressor T-cell)
counts. According to Ravel (1995), the “1993 CDC re-
vised classification system for HIV infection considers
500 CD4 T-cells/mm3 or more to be normal” (p. 273).
CD4/CD8 ratios reduced to less than 1.0 also indicate
immune suppression in the patient infected with HIV.
The normal CD4 count during pregnancy is 700-800
cells/pL, with a normal CD4 to CD8 ratio of 0.9 to 1.92
(Blackburn & Loper, 1992).
Suppression of T-cell activity may lead to
more fulminant disease in pregnant women with
vi raI infections.
The clinical significance of suppression of cell-me-
diated immunity lies in its normal function of protecting
against viral diseases. Pregnant women are known to be
at higher risk of contracting certain viral illnesses and to
experience a more severe course of illness in many cases.
Volume 26, Number 4
 Historically, greater mortality was noted in pregnant
TABLE 3
women with smallpox and with poliomyelitis (Leder-
Normal Laboratory Measures of Immune
man, 1984). In developing countries, viral hepatitis at-
Function During Pregnancy
tacks pregnant women nearly 10 times as frequently as
it does women who are not pregnant, with the greatest I
frequency, morbidity, and mortality noted during the White blood cells 6,000-12,000/mm3
3rd trimester (Lederman, 1984). During influenza epi- Neutrophils 3,800-10,000/mm3
demics, up to 50% of pregnant women were found to Lymphocytes 1,300-5,200/~1~11~
contract pneumonia, with a consequent mortality rate as Monocytes 0-8 00/m3"
high as 27%, twice that of women who were not preg- Eosinophils 0-450/mm3"
nant (Lederman, 1984). Cytomegalovirus in pregnancy CD4 700-800/~1~11~
has been studied heavily because of its association with
CD4:CDS ratio 0.9-1.92
congenital anomalies. The percentage of women with the
Total complement 200-400 mddl
infection who secrete cytomegalovirus from their cervi-
ces increases with gestation, and specific reduction on c3 100-180 mgldl
lymphocyte proliferation against cytomegalovirus oc- Immunoglobulin (1g)A 90-325 mgldl"
curs during the 3rd trimester (Lederman, 1984). Al- IgM 45-150 mgldl"
though pregnant women are not at any higher risk than IgG 700-1,400 mgldl
are other adults to contract varicella, the disease fre- Note. Data from Maternal, Fetal, and Neonatal Physiology, by
quently is more fulminant during pregnancy, bearing a S . T . Blackburn and D. L. Loper, p. 440, 1992, Philadelphia:
higher risk of varicella pneumonia. Mortality rates from W. B. Saunders Co., and Medical Complications DuringPregnancy
by G. N. Burrow and T. F. Ferris, 1995, Philadelphia: W. B. Saun-
varicella pneumonia during pregnancy range from 14% ders Co. Adapted with permission.
to 45% (Branch & Scott, 1994; Lederman, 1984). Preg- a Indicates no change from non-pregnant levels.

nant women who have not had chickenpox should be

instructed to notify their practitioner in the event of ex-
posure. Nurses caring for pregnant women exposed to
varicella should regularly assess respiratory function be-
cause of the increased risk of pneumonia.
Viral diseases exacerbated by pregnancy include
HIV-associated infections, leprosy, coccidioidomycosis,
malaria, and tuberculosis (Wegmann et al., 1993). Preg-
nancy increases susceptibility to hepatitis, rubella, her-
pes, and human papillomavirus, and allows reactivation
of Epstein-Barr and greater replication of viral DNA in
the lower genital tract (Nakamura et al., 1993). In ad-
dition, pregnancy-induced reductions in helper T cells in
HIV-positive women may not resolve after pregnancy
(Nakamura et al., 1993). The information that preg-
nancy can result in an irreversible progression of the dis-
ease should be included when counseling the woman
who is HIV-positive against pregnancy. Tuberculosis
skin tests in pregnant women may not be accurate when
T-cell function is suppressed because T cells are respon-
sible for the local reaction to the injection (see Table 3).
Conclusion
During a normal pregnancy, alterations occur in
virtually every facet of immune response. Enhancements
occur in numbers of circulating PMNs and in humoral
response, leading to more aggressive attack on invading
bacteria. T-cell and NK cell function depression in preg-
nancy and reduced secretion of certain cytokines protect
the fetus and trophoblast from destruction by maternal
immune response. Thus, a general balance between en-
hancement and suppression is achieved, leaving maternal
defenses intact. Nevertheless, T-cell function suppression
increases attack rate, morbidity, and mortality from viral
and opportunistic infections.
T h e perinatal nurse should consider the
normal immunologic changes of pregnancy
when counseling women of childbearing age.
Pregnancy is a normal, healthy state for most
women. The associated immunologic changes usually do
not require major lifestyle changes to protect the
mother's health. However, the perinatal nurse should
consider the normal changes when counseling the preg-
nant woman. By being aware of the normal immune
changes of pregnancy, the perinatal nurse can assess and
educate the patient. The initial prenatal assessment
should include a history of childhood diseases, such as
chickenpox; symptoms of sexually transmitted diseases
and vaginal infections, such as vaginal discharge, ure-
thritis, itching, burning, or lesions; viral illness; and pres-
ence of any immune-mediated diseases, including rheu-
matoid arthritis, systemic lupus erythematosus, and ac-

JulylAugust 1997 JOGNN 393

quired immunodeficiency syndrome. Educating the
patient about increased risks, prevention strategies, and
symptoms can improve pregnancy outcome by allowing
for early medical and nursing intervention.
Considering the ramifications of the normal im-
mune changes of pregnancy, perinatal nurses must un-
derstand normal immune function and the expected
physiologic adaptations of pregnancy. The fetus and the
mother survive and thrive through pregnancy because of
the balance between suppression and enhancement of
the maternal immune system.
REFERENCES
Alberts, B., Bray, D., Lewis, J., Raff, M., Roberts, K., & Wat-
son, J. D. (1983). Molecular biology of the cell. New
York: Garland Publishing, Inc.
Banchereau, J., & Miossec, P. (1993). Role of interleukin-4
and interleukin-5 in allergic disease. In J. J. Oppenheim,
J. L. Rossio, & J. H. Gearing (Eds.), Clinicalapplications
o f cytokines: Role in pathogenesis, diagnosis, and ther-
apy (pp. 245-250). New York: Oxford University Press.
Barriga, C., Rodriguez, A. B., & Ortega, E. (1994). Increased
phagocytic activity of polymorphonuclear leukocytes
during pregnancy. European Journal o f Obstetrics &
Gynecology and Reproductive Biology, 57, 43-46.
Blackburn, S . T., & Loper, D. L. (1992). Maternal, fetal, and
neonatal physiology-A clinical perspective. Philadel-
phia: W. B. Saunders Company.
Branch, D. W., & Scott, J. R. (1994).The immunology of preg-
nancy. In R. K. Creasy & R. Resnik (Eds.), Maternal-
fetal medicine-Principles and practice (3rd ed., pp.
115-127). Philadelphia: W. B. Saunders Company.
Daunter, B. (1992).Immunology of pregnancy: Towards a uni-
fying hypothesis. European Journal of Obstetrics & Gy-
necology and Reproductive Biology, 43, 81-95.
Gibbs, R. S., & Sweet, R. L. (1994). Clinical disorders. In R.
K. Creasy & R. Resnik (Eds.),Maternal fetal medicine-
Principles and practice (3rd ed., pp. 664-665,678-680,
689). Philadelphia: W. B. Saunders Company.
Guyton, A. C. (1991). Textbook of medical physiology (8th
ed.). Philadelphia: W. B. Saunders Company.
394 J O G "
Head, J. R., & Billingham, R. E. (1982). Immunobiological
aspects of the maternal-fetoplacental relationship. In P.
J. Lachmann & D. K. Peters (Eds.), Clinical aspects of
immunology (4th ed., pp. 243-282). London: Blackwell
Scientific Publications.
Larocco, M. (1994). Inflammation and immunity. In C. M.
Porth (Ed.), Pathophysiology: Concepts ofaltered health
states (4th ed., pp. 243-264). Philadelphia: J. B. Lippin-
cott Company.
Lederman, M. M. (1984). Cell-mediated immunity and preg-
nancy. Chest, 86(3), 6s-9s.
Mabie, W. C. (1991). Systemic lupus erythematosus in preg-
nancy. In S. L. Clark, D. B. Cotton, G. D. V. Hankins,
& J. P. Phelan. Critical care obstetrics (2nd ed., pp. 332-
352). Boston: Blackwell Scientific Publications.
Mentlein, R., Staves, R., Rix-Matzen, H., & Tinneberg, H. R.
(1991). Influence of pregnancy on dipeptidyl peptidase
IV activity (CD 26 leukocyte differentiation antigen) of
circulating lymphocytes. European Journal o f Clinical
Chemistry and Clinical Biochemistry, 29(8),477-480.
Nakamura, N., Miyazaki, K., Kitano, Y., Fujisaki, S., & Oka-
mura, H. (1993). Suppression of cytotoxic T-lympho-
cyte activity during human pregnancy. Journal of Re-
productive Immunology, 23,119-130.
Ravel, R. (1995). Clinical laboratory medicine (6th ed.). St.
Louis: Mosby.
Shibuya, T., Isuchi, I., & Kuroiwa, A. (1991). Study on non-
specific immunity in pregnant women: 11. Effect of hor-
mones on chemiluminescence response of peripheral
blood phagocytes. American Journal of Reproductive
Immunology and Microbiology, 26, 76-81.
Wegmann, T. G., Lin, H., Guilbert, L., & Mosmann, T. R.
(1993). Bi-directional cytokine interactions in the ma-
ternal-fetal relationship: Is successful pregnancy a TH2
phenomenon? Immunology Today, 24(7), 353-356.
Wood, G. W. (1994). Is restricted antigen presentation the ex-
planation for fetal allograft survival? Immunology To-
day, 15(1),15-18.
Kristen D. Priddy is a labor and delivery nurse in Fort
Worth, ?x.
Address for cowespondence: Kristen D. Priddy, RNC, MSN,
CNS, 313 Creekside Drive, Hurst, 7'X 76053.
Volume 26, Number 4