Untitled - D Ank Unlimited

delayed xenograft rejection 220 dendritic cells
more macrophages to enter the area, where they become
activated. Skin tests are used clinically to reveal delayed-type
hypersensitivity to infectious disease agents. Skin-test antigens
include such substances as tuberculin, histoplasmin, and candidin.
Tuberculin or purified protein derivative (PPD), which
are extracts of the tubercle bacillus, have long been used to
determine whether a patient has had previous contact with the
organism from which the test antigen was derived. Delayedtype
hypersensitivity reactions are always cell mediated. Thus,
they have a mechanism strikingly different from anaphylaxis
and the Arthus reaction that occur within minutes to hours
following exposure of the host to antigen and are examples
of antibody-mediated reactions. DTH is classified as type IV
hypersensitivity (Coombs and Gell classification). Delayedtype
hypersensitivity may be either permanent, persisting from
a month to years after sensitization (as in classic tuberculintype
hypersensitivity), or transient, resembling the permanent
type morphologically but disappearing 1 to 2 weeks following
induction of sensitization. In the permanent type, the inflammatory
reaction remains prominent 72 to 96 hours following
intradermal injection of antigen, but the inflammatory reaction
disappears 1 to 2 weeks after induction of sensitization in the
transient type, in which the inflammatory lesion peaks at 24
hours but disappears by 48 to 72 hours (Jones–Mote hypersensitivity).
The activation of T cells in DTH is associated
with the secretion of cytokines. Activation of different subsets
of T helper (T H) cells leads to secretion of different types of
cytokines. Those associated with a T H1 CD4 + cellular response
profile include interferon γ (IFN-γ), interleukin-2 (IL2), tumor
necrosis factor β (TNF-β), TNF-α, granulocyte–macrophage
colony-stimulating factor (GM-CSF), and IL3. Cytokines
involved in a T H2 CD4 + cellular response include IL3, IL4,
IL5, IL6, IL10, IL13, TNF-α, and GM-CSF. T H2-type immediate
IgE-mediated hypersensitivity immune responses are
induced by allergens such as animal dander, dust mites, and
pollens, which underlie asthma. Positive tuberculin reactions
induce T H1-type DTH responses associated with T H1 cytokines.
T H1 immunity may possibly inhibit atopic allergies by
repressing T H2 immune responses.
delayed xenograft rejection
Xenograft failure within days to weeks following transplantation.
Attributable to ischemia that is a consequence
of graft vascular endothelium hyperactivation caused by
binding of anti-galactose-α (1-3) galactose antibodies. Also
called acute vascular rejection.
deletional joining
An event during V(D)J recombination; both gene segments
to be brought into apposition have the same transcriptional
orientation.
delivery vehicle
A structure that is both inert and nontoxic and protects
vaccine antigens from degradation by nuclease or protease.
It may serve also as an adjuvant or increase antigen display.
Examples include liposomes, virosomes, ISCOMs, SMAAs,
and biodegradables.
delta agent (hepatitis D virus [HDV])
A viral etiologic agent of hepatitis that is a circular, singlestranded
incomplete RNA virus without an envelope. It is a
1.7-kilobase virus and consists of a small, highly conserved
domain and a larger domain manifesting epitope. HDV is a
subviral satellite of the hepatitis B virus (HBV), on which
it depends to fit its genome into virions. Thus, the patient
must first be infected with HBV to have HDV. Individuals
with the delta agent in their blood are positive for HBsAg,
anti-HBC, and often HBe. This agent is frequently present
in intravenous drug abusers and may appear in patients with
AIDS and in hemophiliacs.
chain
The heavy chain of immunoglobulin D (IgD).
denaturation
Changing the secondary and tertiary structures (coiling
and folding) of a protein to produce a configuration that is
uncoiled or coiled more randomly. Storage causes slow denaturation,
but heating or chemical treatment may induce more
rapid denaturation of native protein molecules. Denaturation
diminishes protein solubility and often abrogates the biologic
activity of the molecule. New or previously unexposed
epitopes may be revealed as a consequence of denaturation.
dendritic cell immunotherapy
The lack of detectable tumor-specific immune responses in
humans led to the use of autologous dendritic cells in active
immunotherapy. Dendritic cells are expanded from progenitors
ex vivo, charged with tumor antigens, and reinfused.
Methods are being sought to genetically modify dendritic
cells with antigens encoded by viral and nonviral vectors.
Dendritic cells might also be used to vaccinate humans at
the time a primary tumor is resected. This would permit an
immune response to be available to act against metastases
not detectable at the time the primary tumor is identified.
dendritic cells
Professional antigen-presenting cells with branched structures
that are powerful activators of T cell responses. They
are bone marrow-derived and distinct from follicular dendritic
cells (DCs) that present antigen to B cells. Immature
DCs are capable of antigen uptake and processing but are
unable to activate T cells. Mature or activated DCs cells
present in secondary lymphoid tissues are able to stimulate
T cells. Subsets are derived from both myeloid and lymphoid
lineages and comprise conventional and plasmacytoid DCs.
Following activation by proinflammatory cytokines, DCs are
attracted to draining lymph nodes where they mature and
upregulate costimulatory molecule expression. Mature DCs
are the only antigen-presenting cells that can activate naïve
T cells. Modulated DCs facilitate development of peripheral
tolerance. Mononuclear phagocytic cells are found in the skin
as Langerhans’ cells, in the lymph nodes as interdigitating
cells, in the paracortex as veiled cells in the marginal sinuses
of afferent lymphatics, and as mononuclear phagocytes in
the spleen, where they present antigen to T lymphocytes.
Dendritic reticular cells may have nonspecific esterase,
Birbeck granules, endogenous peroxidase, possibly CD1,
complement receptors CR1 and CR3, and Fc receptors. DCs
are sentinels of the immune system. They originate from a
bone marrow progenitor, travel through the blood, and are
seeded into non-lymphoid tissues. DCs capture and process
exogenous antigens for presentation as peptide–major histocompatibility
complex (MHC) complexes at cell surfaces and
then migrate via the blood and afferent lymph to secondary
lymph nodes. In the lymph nodes, they interact with T
lymphocytes to facilitate activation of helper and killer T
cells. DCs have been named according to their appearance
and distribution in the body. During the past decade, DCs
have been further characterized by lineage, maturation stage,
functional and phenotype characteristics of these stages, and