Encyclopedia of Health and Medicine

296 The Immune System and Allergies
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 suspicion
of SLE. BLOOD tests 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 conditions
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), antimalarial
medications, CORTICOSTEROID MEDICATIONS,
and IMMUNOSUPPRESSIVE MEDICATIONS. SLE is a
chronic condition that medications can regulate to
permit a relatively normal lifestyle. Stress exacerbates
symptoms and precipitates flareups. Most
people learn to identify when a flareup of symptoms
is pending and to take appropriate interventions
(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 Measures
The main risk factors for SLE are being female and
being African American. Researchers do not know
why gender and ethnicity influence the development
of SLE. Preventive measures focus on reducing
the complications of symptoms through
prompt medical intervention and lifestyle practices,
such as nutritious EATING HABITS and 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 BLOOD cell
(LEUKOCYTE) responsible for CELL-MEDIATED
IMMUNITY. T-cell lymphocytes come to maturity in
the THYMUS during 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 subtypes.
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 CYTOKINES that stimulate B-CELL LYMPHO-
CYTE and cytotoxic T-cell lymphocyte activity
• memory T-cells, which carry specific antibodies
and circulate in the blood for rapid activation
should the same ANTIGEN reappear
• suppressor T-cells, which call off the IMMUNE
RESPONSE when 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
LYMPH. T-cell lymphocytes may also be the source
of disease, such as in HIV/AIDS (the VIRUS attaches to
CD4 helper T-cells) and cutaneous T-cell lymphoma
(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 BLOOD circulation that attach to the surfaces