Untitled - D Ank Unlimited

flame cells 275 FLIP/FLAM
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Polymeric flagellin is an excellent thymus-independent antigen.
Mutations may occur in the central part of a flagellin
monomer, which has a variable sequence.
flame cells
Plasma cells whose cytoplasm stains intensely eosinophilic
and contains glycoprotein globules. Flame cells occur in
immunoglobulin A (IgA) myelomas especially, but also in
Waldenström’s macroglobulinemia and in the leptomeninges
of patients with African trypanosomiasis near neutrophil
aggregates.
flavivirus immunity
Yellow fever, dengue, Japanese encephalitis, and tick-borne
encephalitis are the most important of the flavivirus group.
The E protein plays a critical role in infection and immunity,
as it possesses cellular receptor-binding determinants,
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Ribbon model of FKBP.
Atomic structure of FKBP–rapamycin, an immunophilin–immunosuppressant
complex.
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Flame cell.
Reddish
cytoplasm
membrane fusion activity, and epitopes for neutralizing
antibodies. Macrophages clear the viremia, yet antiviral
function may be affected by their state of activation and
levels of virus-specific antibodies. West Nile virus infection
is associated with impaired natural killer (NK) cell function
that may be related to major histocompatibility complex
(MHC) class I antigen expression on virus-infected cells
and may represent an immune escape mechanism. Virusspecific
antibodies provide protection against flavivirus
disease. Anti-E protein antibodies are protective in various
species and are believed to play a major role in immunity
and natural infections. Previous infections are thought
to ameliorate or protect from subsequent infections with
heterologous viruses by inducing the formation of groupspecific
antibodies. Flavivirus NS1 protein stimulates
protective antibodies. Antibody-dependent cellular cytotoxicity
(ADCC) occurs in dengue fever. Cellular immunity is
believed to be required for control of infection, as T cells
adoptively transferred into unimmunized mice can protect
them against lethal encephalitis. Antibody-enhanced infection
of mononuclear phagocytes occurs in dengue fever.
Primary dengue infection sensitizes serotype cross-reactive
memory T lymphocytes for activation during the secondary
infection, leading to inflammatory cytokine release
that facilitates the development of capillary leak syndrome.
CD4 and CD8 cytotoxic lysis of virus-infected cells has
been observed in dengue fever. Dengue antigen stimulates
CD4 + T cells to synthesize interferon γ. Memory responses
are primed for major activation during secondary infections.
The YF17D strain of yellow fever virus was the first
live-attenuated vaccine for this virus family. It has proven
safe and highly effective for inducing long-lasting immunity.
Other members of this virus group are also candidates
for vaccine development. Tick-borne encephalitis virus
vaccine is a formalin-inactivated preparation that is highly
effective in producing few side effects. Vaccination against
Japanese encephalitis has included both inactivated and live
attenuated viruses.
FLIP/FLAM
FLIP/FLAM is highly homologous to caspase-8. It does
not, however, contain the active site required for proteolytic
activity. FLIP appears to compete with caspase-8 binding to
the cytosolic receptor complex, thereby preventing the activation
of the caspase cascade in response to members of the
tumor necrosis factor (TNF) family of ligands. The exact in
vivo influence of the inhibitor of apoptosis (IAP) family of
protein on apoptosis is not clear.
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