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toxin-1 (TSST-1) 711 TRALI (transfusion-related acute lung injury)
Neutralization does not destroy the reacting toxin. In many
instances, toxin may be recovered by dilution of the toxin–
antitoxin mixture. The effect of heat on a zootoxin is illustrated
by the destruction of cobra venom antitoxin if cobra
venom (toxin)–antivenom (antitoxin) mixtures are subjected
to boiling. The venom or toxin remains intact. Because toxins
have specific affinities for certain tissues, e.g., the high affinity
of tetanus toxin for nervous tissue, antitoxins are believed
to act by binding toxins before they have the opportunity to
combine with specific tissue cell receptors.
toxin-1 (TSST-1)
A toxic bacterial product secreted by Staphylococcus
aureus and implicated in toxic shock syndrome.
Toxocara canis immunity
The human immune response to the domestic dog roundworm
or Toxocara canis includes the development of
antibodies useful for immunodiagnosis to detect infection.
The seroprevalence rate in the United States general
population is 2.8% for adults and 23.1% for children. The
immune response is also characterized by development of
eosinophilic granulomata which may appear throughout the
body except for the brain. Larvae within liver granulomata
may be killed. T. canis infection induces powerful Th2
responses in experimental animals. No vaccine is available.
toxoid
Treatment of a microbial toxin with formaldehyde to inactivate
toxicity while leaving the immunogenicity (antigenicity)
of the preparation intact. Toxoids are prepared from
exotoxins produced in diphtheria and tetanus. They are used
to induce protective immunization against adverse effects
of the exotoxins in question.
toxoid–antitoxin floccules
An immunizing preparation used to induce active immunity
against diphtheria in subjects who are hypersensitive
to alum-precipitated toxoid alone. The preparation consists
of diphtheria toxoid combined with diphtheria antitoxin in
the presence of minimal excess antigen. Horse serum in the
preparation may induce hypersensitivity to horse protein in
some subjects.
Toxoplasma gondii immunity
Both humoral and cell-mediated responses follow infection
with T. gondii. The cellular immune response is the principal
mediator of resistance to infection, although both types of
responses confer resistance. Antibodies activate complement
by the classical pathway to lyse extracellular parasites.
Tachyzoites coated with immunoglobulin within macrophages
are killed. Monocytes and neutrophils also mediate
effective killing. While antibodies mediate only a partial protective
effect, cell-mediated immunity is critical for survival
of the host during acute infection. Activation of macrophages
by interferon-γ (IFN-γ) is a principal effector mechanism in
toxoplasma infection. Macrophages kill by both oxidative
and nonoxidative pathways. Natural killer (NK) and T cells
are essential components of the efferent limb of the protective
cell-mediated immune response. CD8 + T cells produce
IFN-γ to activate macrophages, and CD4 + T cells synthesize
interleukin-2 (IL2), which facilitates IFN-γ synthesis by
CD8 + T cells. NK cells also produce IFN-γ that helps induce
a Th1-type response (IL2 and IFN-γ synthesis) of CD4 +
T cells. Transforming growth factor β (TGF-β) and IL10
downregulate IFN-γ production by NK cells during infection.
AIDS patients may develop toxoplasmic encephalitis,
indicating the significance of their lost cell-mediated
immunity. Tachyzoites in the acute stage of infection are the
principal targets for the protective immune response. They
induce both antigen-specific and nonspecific suppressor cells
to inhibit induction of the immune response to the parasite.
No vaccine for T. gondii is available.
toxoplasmosis
A disease induced by the Toxoplasma gondii protozoan
parasite.
Tp44 (CD28)
A T lymphocyte receptor that regulates cytokine synthesis,
thereby controlling responsiveness to antigen. Its significance
in regulating T lymphocyte activation is demonstrated
by the ability of monoclonal antibody against CD28
receptor to block T cell stimulation by specific antigen.
During antigen-specific activation of T lymphocytes,
stimulation of the CD28 receptor occurs when it combines
with the B7/BB1 coreceptor during the interaction of T and
B lymphocytes. CD28 is a T lymphocyte differentiation
antigen that four fifths of CD3/Ti + lymphocytes express.
It is a member of the immunoglobulin superfamily. CD28
is found only on T lymphocytes and plasma cells. The 134
extracellular amino acids have transmembrane domains and
brief cytoplasmic tails in the CD28 monomers.
TPA
Abbreviation for tissue plasminogen activator.
TPHA
Refer to Treponema pallidum hemagglutination assay.
TPI
Refer to Treponema pallidum immobilization test.
T piece
Refer to secretory piece.
TR1
Refer to regulatory T cell.
Tr1 cells
CD4 + regulatory T cells that secrete IL10 and diminutive
quantities of TGF-β.
trace labeling
Refer to isotopic labeling.
traffic area
Thymus-dependent area.
TRAFs (TNF receptor-associated factors)
Signal transducing molecules composed of at least six
members that bind to various tumor necrosis factor (TNF)
family receptors (TNFRs). They all share a TRAF domain
in common and play a critical role as signal transducers
between upstream members of the TNFR family and downstream
transcription factors.
TRAIL (TNF-related apoptosis-inducing ligand)
A member of the tumor necrosis factor (TNF) family of
cytokines. Several TRAIL receptors have been identified,
including decoy receptors that function to antagonize
TRAIL-induced apoptosis.
TRALI (transfusion-related acute lung injury)
A form of acute respiratory distress syndrome (ARDS),
with a reasonably good prognosis, that often occurs within
hours following a blood transfusion. It is attributable to
leukocyte antibodies and is an acute pulmonary reaction
leading to noncardiac pulmonary edema. Mortality is
10% as opposed to 50 to 60% for other forms of ARDS.
Eighty percent of TRALI patients experience rapid resolution
of pulmonary infiltrates and restoration of arterial
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