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naturally acquired immunity 526 Neisseria immunity
naturally acquired immunity
Immunity that develops as a consequence of unplanned and
coincidental contact with an antigen, as contrasted with
immunity acquired through deliberate immunization.
NCR
Refer to natural cytotoxicity receptor.
necrosis
Cell or tissue death caused by chemical or physical injury
as opposed to apoptosis (biologically programmed cell
death). Necrosis leaves extensive cellular debris that must
be removed by phagocytes; apoptosis does not. “Danger signal”
mediators that initiate inflammation may be released
from necrotic cells.
necrotaxis
The attraction of leukocytes to dead or injured cells and
tissues.
Nef (HIV)
A multifunctional protein in an HIV-infected cell that
forces internalization of certain MHC class I, class II, and
CD4 molecules mediated by clathrin, disturbs the proton
pump needed for endosome acidification, activates intracellular
signaling pathways to induce infected cells to promote
viral DNA synthesis, upregulates FasL, activates caspase-3,
and downregulates survival signaling.
negative induction apoptosis
Negative induction of apoptosis by loss of suppressor activity
involves the mitochondria. Release of cytochrome c
from the mitochondria into the cytosol serves as a trigger to
activate caspases. Permeability of the mitochondrial outer
membrane is essential to initiation of apoptosis through this
pathway. Proteins belonging to the Bcl-2 family appear to
regulate the membrane permeability to ions and possibly
to cytochrome c as well. Although these proteins can form
channels in membranes, the molecular mechanisms by
which they regulate mitochondrial permeability and the
solutes released are less clear. The Bcl-2 family is composed
of a large group of anti-apoptosis members that when
overexpressed prevent apoptosis and pro-apoptosis members
that when overexpressed induce apoptosis. The balance
between the anti- and pro-apoptotic Bcl-2 family members
may be critical to determining whether a cell undergoes
apoptosis. Thus, the suppressor activity of the anti-apoptotic
Bcl-2 family appears to be negated by the pro-apoptotic
members. Many members of the pro-apoptotic Bcl-2 family
are present in cells at levels sufficient to induce apoptosis.
However, these members do not induce apoptosis because
their activity is maintained in a latent form. Bax is present
in the cytosols of live cells. After an appropriate signal,
Bax undergoes a conformational change and moves to the
mitochondrial membrane where it causes release of mitochondrial
cytochrome c into the cytosol. BID is also present
in the cytosols of live cells. After cleavage by caspase-8,
it moves to the mitochondria where it causes release of
cytochrome c, possibly by altering the conformation of
Bax. Similarly, BAK appears to undergo a conformational
change that converts it from an inactive to an active state.
Thus, understanding the molecular mechanisms responsible
for regulating the Bcl-2 family activities creates the potential
for pharmaceutical intervention to control apoptosis.
The viability of many cells is dependent on a constant or
intermittent supply of cytokines or growth factors. In the
absence of an apoptosis-suppressing cytokine, cells may
undergo apoptosis. BAD is a pro-apoptotic member of the
Bcl-2 family and is sequestered in the cytosol when cytokines
are present. Cytokine binding can activate PI3 kinase,
which phosporylates Akt/PKB, which in turn phosphorylates
BAD. Phosphorylated BAD is sequestered in the cytosol
by the 14-3-3 protein. Removal of the cytokine turns the
kinase pathway off, the phosphorylation state of BAD shifts
to the dephosphorylated form, and dephosphorylated BAD
causes release of cytochrome c from the mitochondria.
negative phase
The decrease in antibody titer immediately following injection
of a second or booster dose of antigen to an animal
previously given a primary injection of the same antigen.
Following this initial drop of preformed antibody in the
circulation, there is a rapid and pronounced rise in antibody
titer, representing immunologic memory.
negative selection
The process whereby thymocytes that recognize self antigens
in the context of self major histocompatibility complex
(MHC) undergo clonal deletion (apoptosis) or clonal
anergy (inactivation). The resulting cell population is self
MHC-restricted and self antigen-tolerant (refer to positive
selection). Developing thymocytes in the thymus, whose
TCRs show high affinity/avidity for self-peptide complexed
to self MHC presented by thymic epithelial cells, undergo
apoptosis. Negative selection of NK T cells also occurs in
the thymus. Autoreactive B cells undergo a similar process
in the bone marrow. Autoreactive B cells, whose BCRs have
high affinity/avidity for self antigens present on bone marrow
stromal cells, are induced to undergo apoptosis.
NEHJ pathway
Refer to non-homologous end-joining pathway.
Neisser–Wechsberg phenomenon
The deviation of complement by antibody. Although complement
does not react with antigen alone, it demonstrates
weak affinity for unreacted antibody.
Neisseria immunity
Even though patients with gonococcal infection develop
increased levels of serum and mucosal antibody of immunoglobulin
G (IgG) and IgA classes reactive with gonococcal
surface antigens, they are subject to repeated episodes
of urogenital infections; thus, natural infection does not
confer protective immunity. The surface antigens may be
antigenically heterogeneous or this phenomenon may be
attributable to the brevity of the mucosal antibody response
and the lack of activity of serum antibody in the mucosal
infection. Attachment and colonization of the mucosa with
gonococci during their encounter with polymorphonuclear
neutrophils (PMNs) play important roles. Protective
immunity against meningococcal infection is associated
with complement-dependent, bactericidal serum antibodies
specific for capsular polysaccharide. Cell-mediated
immunity does not appear to have a significant role. There
is no successful gonococcal vaccine. Polysaccharide vaccines
to protect against N. meningitidis of serogroups A and
C induce protective bactericidal antibodies. The current
vaccine contains polysaccharide from serogroups A, C, Y,
and W-135. Polysaccharide A and C vaccine is conjugated
to tetanus toxoid or another protein carrier to enhance
immunogenicity in young children. Polysaccharide vaccines
may not induce protection in serogroup B meningococcal
disease. Protection against these strains may be linked to