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neural cell adhesion molecule L1 (NCAM-L1) 529 neuronal autoantibodies
Epitope on
antigen
B
Anti-idiotype 1
antibody
Paratope
B B
Jerne network theory.
Idiotope
Anti-idiotype 2
antibody
the antigen. Selected anti-idiotypic antibodies have binding
sites similar to the immunizing epitopes known as internal
images of the epitopes. Other anti-idiotypic antibodies are
directed to idiotopes of the antigen-binding region and are
not internal images. Anti-idiotypic antibodies with internal
images may be substituted for an antigen, leading to specific
antigen-binding antibodies. These are the bases for
so-called idiotypic vaccines in which an individual is never
exposed to the infecting agent. Anti-idiotypes may also
block T cell receptors for the corresponding antigen.
Neural cell adhesion molecule L1 (NCAM-L1).
neural cell adhesion molecule L1 (NCAM-L1)
Member of the immunoglobulin gene superfamily.
Although originally identified in the nervous system,
NCAM-L1 is also expressed in hematopoietic and epithelial
cells. It may function in cell–cell and cell–matrix interactions.
It can support homophilic NCAM-L1–NCAM-L1
and integrin cell binding and bind with high affinity to the
neural proteoglycan neurocan. NCAM-L1 promotes neurite
outgrowth by functioning in neurite extension.
neuraminidase
An enzyme that cleaves the glycosidic bond between
neuraminic acid and other sugars. Neuraminic acid is a
critical constituent of multiple cell-surface glycoproteins
and confers a negative charge on the cells. Cells treated with
neuraminidase agglutinate more readily than do normal
cells because of the diminished Coulombic forces between
them. Cells treated with neuraminidase activate the alternate
complement pathway. Neuraminidase is produced by myxoviruses,
paramyxoviruses, and such bacteria as Clostridium
perfringens and Vibrio cholerae. Neuraminidase and hemagglutinin
are found on the spikes of the influenza virus.
neurofilament
A marker, demonstrable by immunoperoxidase staining, for
neural-derived tumors and selected endocrine neoplasms
with neural differentiation.
neurofilament (2F11), mouse antibody
Neurofilament antibody stains an antigen localized in a
number of neural, neuroendocrine, and endocrine tumors.
Neuromas, ganglioneuromas, gangliogliomas, ganglioneuroblastomas,
and neuroblastomas stain positively for
neurofilament. Neurofilament is also present in paragangliomas
and adrenal and extraadrenal pheochromocytomas.
Carcinoids, neuroendocrine carcinomas of the skin, and oat
cell carcinomas of the lung also express neurofilament.
neuroleukin
A cytokine synthesized in the brain and in T lymphocytes
as a 56-kDa protein that shares sequence homology with the
gp120 of HIV-1 and with phosphohexose isomerase. Thus,
the ability of the gp120 of the AIDS virus to compete with
neuroleukin for the neuroleukin receptor may be associated
with AIDS dementia.
neurological autoimmune diseases
Disorders that can alter function of the nerve–muscle junction.
Nerve–muscle junction disorders include myasthenia
gravis and Lambert–Eaton syndrome. Guillain-Barré syndrome
is an example of a peripheral nerve disorder. Multiple
sclerosis and post-infectious vaccination encephalomyelitis
are examples of central nervous system disorders.
neuromuscular junction autoimmunity
The three autoantibody-mediated disorders of the neuromuscular
junction include: (1) myasthenia gravis (MG),
a disorder in which antibodies lead to loss of muscle
acetylcholine receptors (AChRs)—a disease that satisfies
all Witebsky’s criteria for antibody-mediated autoimmune
diseases listed elsewhere in this volume; (2) the Lambert–
Eaton myasthenic syndrome (LEMS), an antibody-mediated
presynaptic disease in which the target is the nerve terminal
voltage-gated calcium channel that meets two of Witebsky’s
criteria; and (3) acquired neuromyotonia (Isaacs’ syndrome),
a disorder induced by autoantibodies against voltage-gated
potassium channels in peripheral motor nerves,
resulting in increased excitability and continuous muscle
fiber activity that satisfies two of Witebsky’s criteria.
neuronal antibodies
Antibodies present in the cerebrospinal fluids of approximately
three fourths of patients who have systemic lupus
erythematosus (SLE) with neuropsychiatric manifestations;
11% of SLE patients who do not manifest neuropsychiatric
disease also develop neuronal antibodies. Neuronal antibodies
are identified by their interactions with human neuroblastoma
cell lines. The presence of neuronal antibodies
generally indicates central nervous system (CNS) SLE. The
lack of neuronal antibodies in the serum and cerebrospinal
fluid mitigates against CNS involvement in SLE patients.
neuronal autoantibodies
Autoantibodies that react with neuroblastoma cell surface
antigens present in 75% of SLE cases with neuropsychiatric
N