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fibrinogen 272 filarial immunity
an event with serious clinical significance. Abzymes, such
as thromboplastin activator linked to an antibody specific
for antigens in fibrin that are not present in fibrinogen, are
used clinically to lyse fibrin clots obstructing coronary
arteries in myocardial infarction patients.
fibrinogen
Fibrinogen is one of the largest plasma proteins, with a
molecular weight of 330 to 340 kDa, and is composed of
more than 3000 amino acid residues. The concentration in
the plasma ranges between 200 and 500 mg/l00 mL. The
molecule contains 3% carbohydrate, about 28 to 29 disulfide
linkages, and one free sulfhydryl group. Fibrinogen exists as
a dimer and can be split into two identical sets composed of
three different polypeptide chains. Fibrinogen is susceptible
to enzymatic cleavage by a variety of enzymes. The three
polypeptide chains of fibrinogen are designated Aα, Bβ, and
γ. By electron microscopy, the dried fibrinogen molecule
shows a linear arrangement of three nodules 50 to 70 Å in
diameter connected by a strand about 15 Å thick.
fibrinoid necrosis
Tissue death in which there is a smudgy eosinophilic deposit
that resembles fibrin microscopically and camouflages
cellular detail. It is induced by proteases released from
neutrophils that digest the tissue and cause fibrin deposition.
Fibrinoid necrosis is seen in tissues in a number of connective
tissue diseases with immune mechanisms. An example
is systemic lupus erythematosus (SLE). Fibrinoid necrosis
is classically seen in the walls of small vessels in immune
complex vasculitis such as occurs in the Arthus reaction.
fibrinopeptides
Peptides released by the conversion of fibrinogen into fibrin.
Thrombin splits fragments from the N terminal regions
of Aα and Bβ chains of fibrinogen. The split fragments
are called fibrinopeptide A and B, respectively, and are
released in the fluid phase. They may be further degraded
and apparently have vasoactive functions. The release rate
of fibrinopeptide A exceeds that of fibrinopeptide B, and
this differential release may play a role in the propensity of
nascent fibrin to polymerize.
fibronectin
An adhesion-promoting dimeric glycoprotein found abundantly
in connective tissues and basement membranes. The
tetrapeptide, Arg–Gly–Asp–Ser, facilitates cell adhesion
to fibrin, Clq, collagens, heparin, and type I-, II-, III-, V-,
and VI-sulfated proteoglycans. Fibronectin is also present
in plasma and on normal cell surfaces. Approximately 20
separate fibronectin chains are known. They are produced
from the fibronectin gene by alternative splicing of the RNA
transcript. Fibronectin is comprised of two 250-kDa subunits
joined near their carboxyl terminal ends by disulfide bonds.
The amino acid residues in the subunits vary in number from
2145 to 2445. Fibronectin is important in contact inhibition,
cell movement in embryos, cell-substrate adhesion, inflammation,
and wound healing. It may also serve as an opsonin.
fibrosis
The formation of fibrous tissue, as in repair or replacement of
parenchymatous elements. A process that leads to the development
of a type of scar tissue at a site of chronic inflammation.
FICA (fluoroimmunocytoadherence)
The use of column chromatography to capture antigenbinding
cells.
ficin
A substance employed to delete sialic acid from cell
surfaces, which is especially useful in blood grouping to
decrease the ζ potential and facilitate otherwise poorly
agglutinating antibodies. Erythrocytes treated with ficin
reveal enhanced expression of Kidd, Ii, Rh, and Lewis
antigens. The treatment destroys MNSs, Lutheran, Duffy,
Chido, Rodgers, and Tn, among other antigens.
Ficoll
A 400-kDa water-soluble polymer composed of sucrose
and epichlorohydrin. It is employed in the manufacture
of Ficoll–Hypaque, a density gradient substance used to
separate and purify mononuclear cells by centrifugation
following removal of the buffy coat.
Plasma
Mononuclear cells
Ficol
Red cells
Schematic representation of Ficoll-Hypaque technique of cell separation.
Ficoll–Hypaque
A density gradient medium used to separate and purify
mononuclear cells by centrifugation.
FIGE
Field inversion gel electrophoresis. Refer to pulsed-field
gradient gel electrophoresis.
filarial immunity
Increased levels of parasite-specific antibodies are synthesized
following filarial infection. Subjects with asymptomatic
microfilaremic infections develop high titers of
filarial-specific immunoglobulin G 4 (IgG 4) antibodies, yet
patients with chronic lymphatic obstruction develop mainly
IgG 1, IgG 2, and IgG 3. Most infected subjects develop antifilarial
IgE antibodies. IgE and IgG4 antibodies are usually
directed against the same epitopes and are regulated by interleukin-4
(IL4) and IL13. Little or no proliferative response to
parasite antigens occurs in lymphocytes from asymptomatic
microfilaremia individuals. This lack of T cell reactivity is
parasite antigen-specific, as responsiveness to nonparasite
antigens and mitogens is unaffected. Asymptomatic microfilaremic
subjects are unable to produce interferon (IFN)
or IFN-γ but retain the ability to synthesize IL4 and IL5.
Subjects with chronic lymphatic pathology synthesize IFN-γ,
IL4, and IL5 following exposure to the parasite antigen. IL10
modulates the synthesis of IFN-γ in microfilaremia. Prenatal
exposure to microfilarial stage antigens can lead to long-term
anergy to filarial antigens once naturally infected. Protective
immunity can be induced by attenuated larvae or by repeated
infections. Individuals who develop resistance to new infection
while maintaining adult parasites acquire concomitant
immunity. The few individuals who remain free of infection
in spite of long-term residence in high endemic areas are said
to have putative immunity.