Untitled - D Ank Unlimited

nuclear matrix protein 537 nutrition and immunity
from the cytosol to the nucleus following cleavage of the
phosphate residues by calcineurin, a serine/threonine protein
phosphatase.
nuclear matrix protein
A marker expressed preferentially by malignant cells
rather than by normal cells; demonstrated by immunoperoxidase
staining.
nuclear matrix proteins (NMPs)
Substances that organize nuclear chromatin. They are
associated with DNA replication, RNA synthesis, and
hormone receptor binding. Antibodies against NMPs react
with nuclear mitotic apparatus protein. Thus, much of the
nuclear matrix is devoted to formation of the mitotic apparatus
(MA). NMPs participate in cellular events that result
in programmed cell death (apoptosis).
nucleolar autoantibodies
Antibodies associated with systemic sclerosis (SSc) include
autoantibodies to nucleolar 7-2 RNA, present in only a
small percentage of patients with SSc; RNA polymerase I,
found in 4% of patients with SSc; the fibrillarin component
of U3 RNP, found in 6% of patients with SSc; and PM-Scl
autoantibodies, found in 3% of polymyositis–scleroderma
overlap syndrome cases. Nucleolar autoantibodies have also
been observed in chronic graft-vs.-host disease following
bone marrow transplantation. Indirect immunofluorescence
is used to demonstrate nucleolar staining patterns that
include speckled or punctuate (RNA polymerase I specificity),
homogeneous (PM-Scl specificity), and clumpy (U3
RNP specificity). Hep-2 cells are useful as a substrate to
detect nucleolar autoantibodies.
nucleoside phosphorylase
An enzyme that is only seldom decreased in immunodeficiency
patients. It catalyzes inosine conversion into
hypoxanthine.
nucleotide excision pathway (NER)
A DNA repair pathway with participation by products of
the XPA-XPG genes capable of excising nucleotides injured
by UV irradiation.
nude mouse
A strain of hairless mouse that has a congenital absence of
the thymus and of T lymphocyte function. An autosomalrecessive
mutation that inhibits hair follicle development
and prevents or greatly diminishes thymus development.
The mice are hairless and lack T cells and serve as highly
effective animal models to investigate the immunologic
consequences of the absence of a thymus. The mice fail to
develop cell-mediated (T-lymphocyte-mediated) immunity,
are unable to reject allografts, and cannot synthesize
antibodies against the majority of antigens. Their B lymphocytes
and natural killer cells are normal even though T
lymphocytes are missing. Also called nu/nu mice. Valuable
in the investigation of graft-vs.-host disease. Partial model
for DiGeorge syndrome in humans.
null cell
A lymphocyte that does not manifest any markers of T or
B cells, including cluster of differentiation (CD) antigens
or surface immunoglobulins. Approximately 20% of
peripheral lymphocytes are null cells. They play a role in
antibody-dependent cell-mediated cytotoxicity (ADCC) and
may be the principal cells in certain malignancies such as
acute lymphocytic leukemia of children. The three types of
null cells include (1) undifferentiated stem cells that may
mature into T or B lymphocytes, (2) cells with labile immunoglobulin
G (IgG) and high affinity Fc receptors that are
resistant to trypsin, and (3) large granular lymphocytes that
constitute natural killer (NK) and killer (K) cells.
null cell compartment
Null cells constitute 37% of the bone marrow lymphocytes
(i.e., they do not have any markers characteristic of B or
T cell lineage). They may differentiate into B or T cells
upon appropriate induction, the mechanism of which is
unknown. Some null cells differentiate into killer (K) cells
by developing Fc and complement receptors. Natural killer
(NK) cells are also present in this cell population. Null, K,
and NK cells, like committed lymphocytes, also migrate to
the peripheral lymphoid organs such as spleen and lymph
nodes, or the thymus, but they represent only a very small
fraction of the total cells present there. At all locations, the
null cells are part of the rapidly renewed pool of immature
cells with short lifespans (5 to 6 days). The null cells committed
to T cell lineage migrate to the thymus to continue
their differentiation.
null phenotype
The failure to express protein because the gene that encodes
it is either defective or absent on both inherited haplotypes.
Most of these involve erythrocytes, but they are quite rare.
nurse cell
Refer to thymus.
nutrition and immunity
The most frequent cause of immunodeficiency worldwide
is malnutrition. Protein energy malnutrition has an adverse
effect on immunity, increases the frequency of opportunistic
infections, and leads to lymphoid tissue atrophy with
reduction in size of the thymus, depletion of lymphoid
cells in thymus-dependent areas of lymph nodes, and a
loss of lymphoid cells around small vessels in the spleen.
It leads to delayed hypersensitivity responses in the skin to
both new and recall antigens. The helper/suppressor ratio
is significantly decreased, and lymphocyte proliferation
and synthesis of DNA are diminished. Serum antibody
responses are usually unaffected. Phagocytosis is affected
as a consequence of decreased complement, component
C3, factor B, and total hemolytic activity. Ingestion by
phagocytes is intact. Metabolic destruction of microorganisms
is decreased, as is synthesis of various cytokines,
including interleukin-2 (IL2) and interferon-γ (IFN-γ).
Deficiency of pyridoxine, folic acid, vitamin A, vitamin C,
and vitamin E leads to impaired cell-mediated immunity
and diminished antibody responses. Vitamin B 6 deficiency
leads to decreased lymphocyte stimulation responses to
mitogens. A moderate increase in vitamin A enhances
immune responses. Zinc deficiency leads to lymphoid
atrophy, decreased cutaneous delayed hypersensitivity
responses and allograft rejection, and diminished thymic
hormone activity. Iron deficiency, the most common nutritional
problem worldwide, leads to impaired lymphocyte
proliferation in response to mitogens and antigens and a
low response to tetanus toxoid and herpes simplex antigens.
Copper-deficient animals have fewer antibody-forming
cells compared to healthy controls. Dietary deficiencies of
selected amino acids diminish antibody responses but in
other states an amino acid imbalance may enhance selected
antibody responses, perhaps reflecting alterations in suppressor
cells.
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