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lymphocytes, circulating (or recirculating) 467 lymphocytotoxic autoantibodies
resting lymphocyte. The transformed cell increases in
size and amount of cytoplasm. Nucleoli develop in the
nucleus, which stains lighter as the cell becomes a blast.
Epstein–Barr virus transforms B cells, and the human
T cell leukemia virus transforms T cells. The lymphocyte
transformation test involves activation of lymphocytes
with mitogens, antigen, superantigens, and antibodies to
components of cell membranes. This leads to their synthesis
of proteins that include immunoglobulins, cytokines, and
growth factors. The activated lymphocyte enters the cell
cycle, synthesizes DNA, replicates, and undergoes metabolic
and morphologic changes. Phytohemagglutinin (PHA)
and concanavalin A (con A), superantigens, anti-CD3 mitogens,
and antigens presented by antigen-presenting cells
activate T lymphocytes. Anti-immunoglobulin, bacterial
lypopolysaccharides, and staphylococcal protein A activate
B lymphocytes. The lymphocyte transformation assay is a
broadly used in vitro test to evaluate lymphocyte function.
lymphocytes, circulating (or recirculating)
The lymphocytes present in the systemic circulation
represent a mixture of cells derived from different sources:
(1) B and T cells exiting from bone marrow and thymus
on their way to seed the peripheral lymphoid organs;
(2) lymphocytes exiting the lymph nodes via lymphatics,
collected by the thoracic duct, and discharged into
the superior vena cava; and (3) lymphocytes derived from
direct discharge into the vascular sinuses of the spleen.
About 70% of cells in the circulating pool are recirculating,
that is, they undergo a cycle during which they exit the
systemic circulation to return back to lymphoid follicles,
lymph nodes, and spleen and start the cycle again. The cells
in the recirculating pool are mostly long-lived mature T
cells. About 30% of the lymphocytes of the intravascular
pool do not recirculate. They comprise mostly short-lived
immature T cells that live their lifespans intravascularly
or are activated and exit the intravascular space. The exit
of lymphocytes into the spleen occurs by direct discharge
from the blood vessels. In lymph nodes and lymphoid follicles,
the exit of lymphocytes occurs through specialized
structures called postcapillary venules. These differ from
other venules in that they have tall endothelial coverings.
The exiting lymphocytes percolate through the endothelial
cells, a mechanism whose significance is not known. A
number of agents such as cortisone or Bordetella pertussis
bacteria increase the extravascular exit of lymphocytes and
prevent their return to circulation. The lymphocytes travel
back and forth between the blood and lymph. They attach to
and pass through the high endothelial cells of the postcapillary
venules of lymph nodes or the marginal sinuses of the
spleen. Within 24 to 48 hours they return via the lymphatics
to the thoracic duct, where they then reenter the blood.
lymphocytic choriomeningitis (LCM)
A murine viral disease that produces inflammatory brain
lesions in affected mice as a result of delayed-type hypersensitivity
to viral antigens on brain cells infected with the
LCM virus. This infectious agent, classified as an arenavirus,
is endemic in the mouse population and occasionally
occurs in humans. Only adult mice that become infected
develop the lesions; those infected in utero are rendered
immunologically tolerant to the viral antigens and fail to
develop disease. An adult with an intact immune system
exposed to LCM virus becomes immune or succumbs to the
acute infection, which is associated with lymphadenopathy,
splenomegaly, and T lymphocyte perivascular infiltration
of the viscera, especially the brain. A chronic carrier state
can be induced in neonatal mice or those with impaired
immune systems through infection with the virus. Although
carriers generate significant quantities of antiviral antibodies,
the infection persists, and virus–antibody immune
complexes become deposited in the renal glomeruli, walls
of arteries, liver, lungs, and heart. The passive transfer of
cytotoxic T lymphocytes from an immune animal to a carrier
results in specific reactivity against LCM viral epitopes
on cell membranes in the brain and meninges, which
leads to profound inflammation and death. Transmission
of this disease is via the excrement of rodents and is seen
especially in winter when rodents enter dwellings. Fever,
headache, flu-like symptoms, and lymphocytosis in the
cerebrospinal fluid are present, as may be associated
leukopenia and thrombocytopenia. This disease must be
distinguished from infectious mononucleosis, herpes zoster,
and enterovirus infection.
Lymphocytic interstitial pneumonia (LIP) with organization.
lymphocytic interstitial pneumonia (LIP)
A diffuse pulmonary disease of middle-aged females who
may also have Sjögren’s disease, hypergammaglobulinemia,
or hypogammaglobulinemia. They develop shortness of
breath, and reticulonodular infiltrates appear on chest films.
Mature lymphocytes and plasma cells appear in the nodular
interstitial changes in alveolar and interlobular septae with
perivascular accumulation of round cells. LIP may resemble
lymphoma based on the monotonous accumulation of small
lymphocytes, and patients may ultimately develop end-stage
lung disease or lymphoma.
lymphocytic leukemia
A malignancy in which abnormal proliferation of transformed
T or B cells manifests a mature peripheral cell phenotype.
lymphocytopenic center
Refer to germinal center.
lymphocytosis
An elevated number of peripheral blood lymphocytes.
lymphocytotoxic autoantibodies
A heterogeneous group of autoantibodies including
(1) those that occur naturally and in selected diseases, are of
the immunoglobulin M (IgM) isotype, and are cold-reactive
at temperatures near 15ºC; (2) lymphocytotoxic autoantibodies
associated with infections such as mumps, herpes,
mycoplasma, chronic parasitic infections, and autoimmune
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