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Foxp3 282 Francisella immunity
which is frequently used to treat cytomegalovirus
infection.
Foxp3
A member of the forkhead/winged helix family of transcriptional
regulators that act as master regulators in regulatory
T cell development and function. Human FOXP3 genes
contain eleven coding exons. The FOXP3 gene maps to
chromosome Xp11.23. In IPEX, the X-linked syndrome of
immunodysregulation, polyendocrinopathy, and enteropathy,
the FOXP3 gene is mutated. The mutations occur in the
forkhead domain of FOXP3, suggesting that the mutations
may disrupt critical DNA interactions. A Foxp3 mutation,
consisting of a frameshift mutation that results in protein
lacking the forkhead domain, leads to “scurfy” in mice.
This is an X-linked recessive mouse mutant that is lethal
in hemizygous males 16 to 25 days after birth. These mice
have over-proliferation of CD4+ T lymphocytes, extensive
multiorgan infiltration, and increases in multiple cytokines.
This phenotype resembles the lack of expression
of CTLA-4, TGF-beta, human disease IPEX, or deletion
of the Foxp3 gene in mice. The pathology in scurfy mice
is apparently a consequence of the inability to regulate
properly CD4+ T cell function. Mice over-expressing the
Foxp3 gene have diminished numbers of T cells that reveal
poor proliferative and cytolytic responses and only weak
IL2 production even though thymic development is normal.
Histologically, the peripheral lymphoid organs, especially
lymph nodes, lack cells.
F:P ratio
Fluorescence-to-protein ratio that expresses the ratio of
fluorochrome to protein in an antibody preparation labeled
with the fluorochrome.
FPR
N-formyl peptide receptor (FPR) is a member of the G
protein-coupled receptor family, the chemokine receptor
branch of the rhodopsin family. Tissue sources include
HL-60 cells differentiated with Bt2 cAMP. Undifferentiated
HL-60 cells transfected with FPR bound FMLP with two
affinities. COS7 cells transfected with FPR bound FMLPK-
Pep12 with low and high affinity. The receptor is expressed
in neutrophils. Dibutyryl cAMP includes FPR transcription
in HL-60 cells.
Fracastoro, Girolamo (1478–1553)
A physician who was born in Verona and educated at
Padua. His interests ranged from poetry to geography.
He proposed the theory of acquired immunity and was a
leader in the early theories of contagion. (Refer to Syphilis
sive Morbus Gallicus, 1530; De Sympathia et Antipathia
Rerum, 1546; De Contagione, 1546.)
fractional catabolic rate
The total plasma immunoglobulin percentage catabolized
daily. Predicted from the half-life of plasma or from the excretion
rate of catabolized immunoglobulin products in urine.
fragmentins
Serine esterases present in cytotoxic T cell and natural
killer cell cytoplasmic granules. The introduction of
fragmentins into the cytosol of a cell causes apoptosis as
the DNA in the nucleus is fragmented into 200-base-pair
multimers. Also called granzymes.
framework regions (FRs)
Relatively invariant regions within variable domains of
immunoglobulins and T cell receptors that constitute a
Girolamo Fracastoro.
protein scaffold for hypervariable regions interacting
with antigen. Amino acid sequences in variable regions
of heavy or light immunoglobulin chains other than the
hypervariable sequences. There is much less variability
in the framework region than in the hypervariable region.
Two β-pleated sheets opposing one another comprise the
structural features of the framework regions of an antibody
domain. Polypeptide chain loops join the β-pleated sheet
strands. The framework regions contribute to the secondary
and tertiary structures of the variable region domain,
although they are less significant than the hypervariable
regions for the antigen-binding site. The framework region
forms the folding part of the immunoglobulin molecule.
Light chain FRs are found at amino acid residues 1 to 28,
38 to 50, 56 to 89, and 97 to 107. Heavy chain FRs are
present at amino acid residues 1 to 31, 35 to 49, 66 to 101,
and 110 to 117.
Francisella immunity
The causative agent of tularemia, Francisella tularensis, may
induce two forms of the disease: ulceroglandular tularemia,
borne by vectors or induced by contact with infected
animals, and respiratory tularemia, caused by inhalation of
contaminated dust. A powerful antibody response occurs
during infection with this microorganism and is detectable
by agglutination, ELISA, or other techniques. The antibodies
appear at the end of the second or during the third week of
infection. They persist for several years following recovery.
Immunoglobulin M (IgM) antibodies do not appear before
IgG antibodies and may even be present for years following
recovery. Cell-mediated immunity in tularemia is demonstrated
by a delayed-type hypersensitivity test or by in vitro
activation of T cells. Cell-mediated immunity against F.
tularensis is requisite for host protection. The microorganism’s
capsule protects it against lysis by complement and
affords resistance to intracellular killing by polymorphonuclear
leukocytes. Attenuated strains of the microorganism,