The diagnostic path is one of exclusion. It can
take months to years for doctors to rule out other
causes of the symptoms and settle on the suspi-
cion of SLE. BLOODtests that detect antinuclear
antibodies (ANAs) suggest SLE. Many people who
have SLE also have other antibodies, including
anti-Ro and anti-La. However, not all do, and
some people have these antibodies and do not
have SLE. Some people who have SLE have
decreased complement factors, though other con-
ditions can cause the same finding.
Treatment Options and Outlook
Treatment incorporates various medications,
singly or in combination, that target symptoms.
The most commonly used medications are NON-
STEROIDAL ANTI-INFLAMMATORY DRUGS(NSAIDS), anti-
malarial medications, CORTICOSTEROID MEDICATIONS,
and IMMUNOSUPPRESSIVE MEDICATIONS. SLE is a
chronic condition that medications can regulate to
permit a relatively normal lifestyle. Stress exacer-
bates symptoms and precipitates flareups. Most
people learn to identify when a flareup of symp-
toms is pending and to take appropriate interven-
tions (medications and relaxation techniques) to
mitigate their effects.
MEDICATIONS TO TREAT
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
cyclophosphamide dexamethasone
hydrocortisone hydroxychloroquine
ibuprofen methotrexate
mycophenolate mofetil naproxen
prednisone
Risk Factors and Preventive MeasuresThe main risk factors for SLE are being female and
being African American. Researchers do not know
why gender and ethnicity influence the develop-
ment of SLE. Preventive measures focus on reduc-
ing the complications of symptoms through
prompt medical intervention and lifestyle prac-
tices, such as nutritious EATING HABITSand daily
physical activity, that support health.
See also ANTIBODY; AUTOIMMUNE DISORDERS; DIS-
COID LUPUS ERYTHEMATOSUS (DLE); LIVING WITH
IMMUNE DISORDERS; LYMPH NODE; MIND–BODY CONNEC-
TION.
T-cell lymphocyte The type of white BLOODcell
(LEUKOCYTE) responsible for CELL-MEDIATED
IMMUNITY. T-cell lymphocytes come to maturity in
the THYMUSduring childhood, which is why they
are called T-cells. During the maturation process,
T-cell lymphocytes “learn” how to recognize self
and nonself antigens so they can distinguish
between cells that belong to the body and cells
that are foreign. Such a safeguard is necessary to
keep T-cell lymphocytes from attacking the body’s
own cells. The thymus destroys lymphocytes that
do not learn this distinction. After the thymus
releases mature T-cell lymphocytes into the blood
circulation, they differentiate into several sub-
types. These include- cytotoxic T-cell lymphocytes, also called killer
T-cells or CD8 cells, which respond to nonself
antigens to kill the cells that bear them - helper T-cells, also called CD4 cells, which
release CYTOKINESthat stimulate B-CELL LYMPHO-
CYTEand cytotoxic T-cell lymphocyte activity - memory T-cells, which carry specific antibodies
and circulate in the blood for rapid activation
should the same ANTIGENreappear - suppressor T-cells, which call off the IMMUNE
RESPONSEwhen the threat to the body ends
The SPLEEN, the lymph nodes, and the MUCOSA-
ASSOCIATED LYMPHATIC TISSUE(MALT) throughout the
body contain millions of T-cell lymphocytes. T-cell
lymphocytes also circulate in the blood and the
LY M P H. T-cell lymphocytes may also be the source
of disease, such as in HIV/AIDS(the VIRUSattaches to
CD4 helper T-cells) and cutaneous T-cell lym-
phoma (CTCL), a form of cancer.
For further discussion of T-cell lymphocytes
within the context of the structures and functions
of the immune system, please see the overview
section “The Immune System and Allergies.”
See also ANTIBODY; ANTIBODY-MEDIATED IMMUNITY;
CLUSTERS OF DIFFERENTIATION; LYMPH NODE; MAJOR HIS-
TOCOMPATIBILITY COMPLEX(MHC); NATURAL KILLER(NK)
CELL.transforming growth factors (TGFs) CYTOKINES
in the BLOODcirculation that attach to the surfaces296 The Immune System and Allergies