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polyagglutination 581 polyclonal lymphocyte activator
proteins, and autoradiography is used to detect radiolabeled
proteins. The molecular weight of an unknown protein can
be predicted using standard proteins for comparison.
polyagglutination
The aggregation of erythrocytes by antibodies, autoagglutinins,
or alloagglutinins in blood serum. Polyagglutination
also refers to aggregation of normal red blood cells treated
with neuraminidase and to red blood cells with altered membranes
that are improperly aggregated by anti-A or anti-B
antibodies. This is linked to altered glycoproteins such as Tn,
T, and Cad. Acquired B antigens may also lead to polyagglutination,
as can bacterial infections. Serum contaminants
including detergents, microbes, metal cations, or silica may
also cause polyagglutination. Also called panagglutination.
polyarteritis nodosa
A necrotizing vasculitis of small- and medium-sized muscular
arteries that often involves renal and visceral arteries
and spares the pulmonary circulation. The disease is often
characterized by immune complex deposition in arteries
and is often associated with chronic hepatitis B virus
infection. Early lesions of the vessels often reveal hepatitis
B surface antigen, IgM, and complement components. This
uncommon disease has a male-to-female ratio of 2.5 to 1.
The mean age at onset is 45 years. Characteristically, the
kidneys, heart, abdominal organs, and both peripheral and
central nervous systems are involved. Lesions of vessels are
segmental and show preference for branching and bifurcation
in small- and medium-sized muscular arteries. Usually,
the venules and veins are unaffected and only rarely are
granulomas formed. Characteristically, aneurysms form following
destruction of the media and internal elastic lamina.
There is proliferation of the endothelium with degeneration
of the vessel wall and fibrinoid necrosis, thrombosis, ischemia,
and infarction. Polyarteritis nodosa is also associated
with tuberculosis, streptococcal infections, and otitis media.
Presenting signs and symptoms include weakness, abdominal
pain, leg pain, fever, cough, and neurologic symptoms.
There may be kidney involvement, arthritis, arthralgia, or
myalgia, and hypertension. Forty percent of patients may
have skin involvement manifested as a maculopapular rash.
Laboratory findings include elevated erythrocyte sedimentation
rate, leukocytosis, anemia, thrombocytosis, and
cellular casts in the urinary sediment signifying renal glomerular
disease. Angiography is important in revealing the
presence of aneurysm and changes in vessel caliber. There
is no diagnostic immunologic test, but immune complexes,
cryoglobulins, rheumatoid factor, and diminished complement
component levels are often found. Biopsies may be
taken from skeletal muscle or nerves for diagnostic purposes.
Corticosteroids may be used, but cyclophosphamide
is the treatment of choice in the severe progressive form.
polyarthritis
Multiple joint inflammation as occurs in rheumatic fever,
systemic lupus erythematosus, and related diseases.
polyclonal
Originating from multiple clones.
polyclonal activators
Agents that stimulate numerous lymphocytes without
regard to their antigen specificity. The proliferating cells
yield products such as immunoglobulins or cytokines.
The proliferating cells lack cell-to-cell collaboration that
reduces mutations in polyclonal activators. Polyclonal
activators use different activation pathways than antigenstimulated
lymphocytes, although pathways overlap and
interact. Numerous polyclonal activators have different
mechanisms of action on cells of immune systems. Among
the polyclonal activators are mitogenic lectins that bind the
polysaccharides of surface structures such as phytohemagglutinin
(PHA), concanavalin A (con A), and pokeweed
mitogen (PWM); bacterial cell wall products that bind
lymphocyte receptors such as lipopolysaccharide (LPS);
calcium ionophores that alter calcium signals; phosphorylation
modifiers that increase stimulatory phosphorylation
events such as phorbol myristate acetate; antigen–receptor
ligands that bind to nonvariable parts of the receptor
mechanism such as staphylococcal protein A; ligands for
costimulatory molecules that bind to lymphocytes and
favor stimulation such as anti-CD40 and CD40L; and
transforming agents that infect cells and cause continued
growth or activation such as HIV. Monoclonal activators
can be used to access the functional status of a particular
lymphocyte population. Some polyclonal activators require
more than one type of cell and may even induce inhibition
and inactivation of lymphocytes. Numerous interactions
occur between antigen-specific and polyclonal forms of
lymphocyte activation and inactivation. Costimulation and
coinhibition regulate specific immune responses. Defects in
signals in these various interactions, especially defects in
signaling associated with antagonism and coinhibition, may
predispose to autoimmune disease.
polyclonal antibodies
Multiple immunoglobulin responding to different epitopes
on an antigen molecule. This multiple stimulation leads to
the expansion of several antibody-forming clones whose
products represent a mixture of immunoglobulins in contrast
to proliferation of a single clone that yields a homogeneous
monoclonal antibody product. Polyclonal antibodies
represent the natural consequence of an immune response
in contrast to monoclonal antibodies that occur in vivo
in pathologic conditions such as multiple myeloma or are
produced artificially by hybridoma technology against one
of a variety of antigens.
polyclonal antiserum
Serum that possesses antibodies synthesized by different B
cell clones following stimulation by an antigen. Different
epitopes on the antigen molecule stimulate this multiplicity
of antibodies.
polyclonal hypergammaglobulinemia
An elevation in the blood plasma of γ globulin due to
increased quantities of the different immunoglobulin classes
rather than an increase of only one immunoglobulin class.
polyclonal lymphocyte activator
Stimulates human lymphocytes. Among the B lymphocytes
stimulated are self-reactive ones that are anergic.
Lipopolysaccharide (LPS) injection may result in the
production of many autoantibodies in mice. Superantigens
may cause polyclonal T cell stimulation, which has been
suggested to be a mechanism for autoimmunity, but evidence
is lacking. Graft-vs.-host reactivity also has many
autoimmune-like features. Response of the human body to
microbial antigens may lead to an immune response that
cross reacts with self antigens. For example, antibodies to
streptococci in rheumatic fever may cross react with antigens
of the myocardium in humans, leading to myocarditis.
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