Untitled - D Ank Unlimited

peripheral lymphoid tissues 566 peroxidase–antiperoxidase (PAP)
peripheral lymphoid tissues
Refer to secondary lymphoid tissues.
peripheral tolerance
Suppression of the function or deletion of self-reactive
lymphocytes that escaped destruction during the development
of central tolerance. Mediated by a variety of means
acting outside the thymus and bone marrow. Among
these are peripheral clonal deletion, anergization, clonal
exhaustion, immunological ignorance, immune privilege,
immunosuppressive cytokines, immune deviation, and
regulatory T cells. Inhibition of expression of the immune
response. The cells delivering the response are functionally
impaired but not defective. Peripheral tolerance
affects the efferent limb of the immune response, which is
concerned with the generation of effector cells. Peripheral
tolerance is acquired by mature lymphocytes in peripheral
tissues. It is induced by recognition of antigens without
sufficient levels of costimulators required for lymphocyte
activation or by persistent and repeated stimulation
by these self antigens (refer to immunologic tolerance).
Mechanisms that interfere with maturation or stimulation
of lymphocytes with the potential for reacting with self
include self tolerance, which is acquired and not inherited.
Lymphocytes reactive with self may be inhibited
from responding to self or inactivated upon combination
with self antigens. Self tolerance may involve both central
and peripheral tolerance. In central tolerance, immature
lymphocytes capable of reacting with self encounter self
antigen, producing tolerance instead of activation. By
contrast, peripheral tolerance involves the interaction of
mature self-reactive lymphocytes with self antigens in
peripheral tissues under conditions that promote tolerance
instead of activation. Clonal deletion and clonal anergy
are also principal mechanisms of tolerance in clones of
lymphocytes reactive with self antigens.
peripheral-type benzodiazepine receptor (PBR)
An 18-kDa protein found in most steroidogenic tissues. It
is found in the outer mitochondrial membrane in association
with a 34-kDa, voltage-dependent anion channel
(VDAC) protein. PBR is thought to be part of the mitochondrial
permeability transition pore and to be involved
in apoptosis.
peripolesis
A gathering of cells of one type around another kind of
cell, such as the accumulation of lymphocytes around
macrophages. This facilitates cell-to-cell interaction in the
induction of an immune response.
peritoneal exudate cells (PECs)
Inflammatory cells resident in the peritoneum of experimental
animals following the interperitoneal injection of an
inflammatory agent such as glycogen, peptone, or paraffin
oil. The cell population varies with time after inoculation.
The first cells to appear are polymorphonuclear neutrophilic
leukocytes, found several hours following injection.
These are followed by lymphocytes and, within 72 hours,
by macrophages. The desired population of cells such as
macrophages may be harvested by peritoneal lavage with an
appropriate tissue culture medium.
permeability factors
Refer to vascular permeability factors.
permeability-increasing factor
A lymphokine that enhances the permeability of vessels.
Absorbed
from gut
I. Normal II. Pernicious anemia
Diet Diet
Stomach Stomach
Parietal cell
Not
absorbed
Plasma cell
B 12 vitamin Intrinsic factor
Pernicious anemia.
Macrocytic anemia.
Macrocyte
Normal RBC
Nucleated RBC
Multilobed PMN
nucleus
pernicious anemia (PA)
An autoimmune disease characterized by the development
of atrophic gastritis, achlorhydria, decreased synthesis of
intrinsic factor, and malabsorption of vitamin B 12. Patients
present with megaloblastic anemia caused by the vitamin
B 12 deficiency. The majority of pernicious anemia patients
develop antiparietal cell antibodies, and at least half of
them also develop antibodies against intrinsic factor, which
is necessary for the absorption of B 12. The antiparietal cell
antibodies are against a microsomal antigen found in gastric
parietal cells. Intrinsic factor is a 60-kDa substance that
links to vitamin B 12 and aids its uptake in the small intestine.
PA may be a complication of common variable immunodeficiency
or may be associated with autoimmune thyroiditis.
PA is caused principally by injury to the stomach mediated
by T lymphocytes. Patients may manifest megaloblastic
anemia, deficiency of vitamin B 12, and increased gastrin in
serum.
peroxidase–antiperoxidase (PAP)
A technique that employs unlabeled antibodies and a PAP
reagent and has proven highly successful for the demonstration
of antigens in paraffin-embedded tissues as an aid
in surgical pathologic diagnosis. Tissue sections preserved
in paraffin are first treated with xylene, and after deparaffinization
are exposed to hydrogen peroxide solution that
destroys the endogenous peroxidase activity in tissue. The
sections are next incubated with normal swine serum,
which suppresses nonspecific binding of immunoglobulin