Untitled - D Ank Unlimited

Farr technique 265 Fasciola immunity
BSA
+
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Radiolabeled
BSA
in the alveolar wall of the lung. This leads to inflammation
that impairs gas exchange by the lungs. Patients become
breathless within hours after inhaling the dust and may
develop interstitial pneumonitis with cellular infiltration of
the alveolar walls where monocytes and lymphocytes are
prominent. This may lead to pulmonary fibrosis following
chronic inflammation, peribronchiolar granulomatous
reaction, and foreign-body-type giant cell reactions.
Corticosteroids are used for treatment. Interaction of the
immunoglobulin G (IgG) antibodies with the inhaled allergen
in the alveoli wall of the lung leads to inflammation
and compromised gas exchange.
Farr technique
An assay to measure primary binding of antibody with
antigen as opposed to secondary manifestations of
antibody–antigen interactions such as precipitation, agglutination,
etc. It is a quantitation of an antiserum’s antigenbinding
properties and is appropriate for antibodies of all
immunoglobulin classes and subclasses. The technique is
limited to the assay of antibody against antigens soluble
in 40% saturated ammonium sulfate solution, in which
antibodies precipitate. Following interaction of antibody
with radiolabeled antigen, precipitation in ammonium
sulfate separates the bound antigen from the free antigen.
The quantity of radiolabeled antigen that has reacted with
antibody can be measured in the precipitate. The antibody
dilution that precipitates part of the ligand reflects the
antigen-binding ability.
Fas
Fas (AP0-1/CD95) is a member of the tumor necrosis factor
(TNF) receptor superfamily. Fas ligand (FasL) is a member
of the TNF family of type 2 membrane proteins. Soluble
FasL can be produced by proteolysis of membrane-associated
Fas. Ligation of Fas by FasL or anti-Fas antibody can
induce apoptotic cell death in cells expressing Fas. Fas is
a member of the TNF receptor family that is expressed on
selected cells, including T cells, and renders them susceptible
to apoptotic death mediated by cells expressing Fas
ligand, a member of the TNF family of proteins on the cell
surface.
Fas ligand
Binding to Fas initiates the death pathway of apotosis in
Fas-bearing cells. Fas-mediated killing of T lymphocytes
is critical for the maintenance of self tolerance. Fas gene
mutations can lead to systemic autoimmune disease. Fas
ligand (FasL) is a member of the tumor necrosis factor
Saline solution
Farr technique.
Anti-BSA
50% Saturated
ammonium sulfate
solution
(TNF) family of proteins expressed on the cell surfaces of
activated T lymphocytes. Binding of FasL to Fas initiates
the signaling pathway that leads to apoptotic cell death of
the cell expressing Fas. FasL gene mutations may lead to
systemic autoimmune disease in mice.
Fas pathway
An apoptotic pathway leading to death of Fas-expressing
cells, which is induced by ligation of the death receptor Fas
by FasL. FADD, caspase-8 and the caspase-3 cascade mediate
signal transduction of this pathway.
fascin (55k-2), mouse
Fascin is a very sensitive marker for Reed–Sternberg cells
and variants in nodular sclerosis, mixed cellularity and
lymphocyte depletion Hodgkin disease. It is uniformly
negative in lymphoid cells, plasma cells, and myeloid
cells. Fascin is positive in dendritic cells. This marker
may be helpful in distinguishing between Hodgkin disease
and non-Hodgkin lymphoma in difficult cases. Also, the
lack of expression of fascin in the neoplastic follicles
in follicular lymphoma can be helpful in distinguishing
these lymphomas from reactive follicular hyperplasia in
which the number of follicular dendritic cells is normal or
increased.
Fasciola immunity
An inflammatory response in the liver is associated with
primary infection of a host with the liver fluke Fasciola
hepatica. The cellular infiltrate includes neutrophils,
eosinophils, lymphocytes, and macrophages. A significant
eosinophilia occurs in the peritoneal cavity and the blood.
There is no cellular response encircling the juvenile flukes.
Numerous macrophages and fibroblasts occur in injured
areas in the chronic phase of a primary infection. This is
followed by liver fibrosis, which is accompanied by numerous
CD8 + and αβ-TCR + T cells. Numerous lymphocytes
and eosinophils infiltrate larger bile ducts, and in cattle a
granulomatous reaction is followed by bile duct calcification.
Resistance to reinfection follows primary infection
of cattle, rats, and possibly humans, but fails to occur in
sheep and mice. The failure of sheep to develop resistance
against reinfection may be associated with cellular immune
deficiencies. Products released from F. hepatica may
adversely affect the host immune response, such as cathepsin
proteases, which flukes secrete and which may cleave
immunoglobulins, thereby inhibiting attachment to host
effector cells. Other immunosuppressive molecules may be
toxic to host cells.
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