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adenosine deaminase (ADA) 19 adhesion proteins
clinical states associated with hypoxia, the α adenosine
level increases five- to ten-fold, suggesting that it may play a
role in the release of mediators. Experimentally, adenosine
is a powerful potentiator of mast cell function. The incubation
of mast cells with adenosine does not induce the release
of mediators. However, by preincubation with adenosine
and subsequent challenge with a mediator-releasing agent,
the response is markedly enhanced.
adenosine deaminase (ADA)
A 38-kDa deaminating enzyme that prevents increased levels
of adenosine, adenosine trisphosphate (ATP), deoxyadenosine,
deoxy-ATP, and S-adenosyl homocysteine. It is encoded
by the chromosome 20q13-ter gene. Elevated adenosine
levels block DNA methylation within cells, leading to their
death. Increased levels of deoxy-ATP block ribonucleosidediphosphate
reductase, which participates in the synthesis
of purines. The absence of adenosine deaminase (ADA)
enzyme, which participates in purine metabolism, causes
toxic purine nucleosides and nucleotides to accumulate, leading
to the deaths of developing thymic lymphocytes.
N
HC
HOCH2 H
H
HO
NH 2
C
C
N
HN
CH
N
C
N
HC
O ADA
deficiency HOCH2 O
H
H H
H
Adenosine
OH HO
Adenosine
deaminase
ADA deficiency.
OH
adenosine deaminase (ADA) deficiency
A form of severe combined immunodeficiency (SCID)
in which affected individuals lack an enzyme, adenosine
deaminase (ADA), which catalyzes the deamination of
adenosine as well as deoxyadenosine to produce inosine and
deoxyinosine, respectively. Cells of the thymus, spleen, and
lymph nodes and red blood cells contain free ADA enzyme.
In contrast to the other forms of SCID, children with ADA
deficiency possess Hassall’s corpuscles in the thymus. The
accumulation of deoxyribonucleotides in various tissues,
especially thymic cells, is toxic and is believed to be a cause
of immunodeficiency. As deoxyadenosine and deoxy-ATP
accumulate, the latter substance inhibits ribonucleotide
reductase activity, which inhibits formation of the substrate
needed for synthesis of DNA. These toxic substances are
especially injurious to T lymphocytes. Autosomal recessive
ADA deficiency leads to death. Two fifths of SCID cases
are of this type. The patient’s signs and symptoms reflect
defective cellular immunity with oral candidiasis, persistent
diarrhea, failure to thrive, and other disorders, with death
occurring prior to 2 years of age. T lymphocytes are significantly
diminished. Eosinophilia and elevated serum and
urine adenosine and deoxyadenosine levels are present. As
bone marrow transplantation is relatively ineffective, gene
therapy is the treatment of choice.
O
C
N
C
C
Inosine
N
N
H
CH
adenovirus infection and immunity
Species-specific icosahedral DNA viruses that belong to
numerous serotypes. They produce multiple clinical syndromes
in humans including respiratory, genitourinary, gastrointestinal,
and conjunctival infections. They are resistant to
most antiviral chemotherapy. An oral vaccine has been very
successful in preventing acute respiratory disease in military
personnel. Humans develop serotype-specific neutralizing
antibodies to the structural proteins, thereby preventing reinfection
with the same serotype. Early (E) nonstructural proteins
produce significant immunologic effects. The virus has
a double-stranded linear DNA and more than 12 structural
proteins. There is no virus envelope. The viral polypeptides
serve as antigens for host immune responses generated as a
consequence of infection or as a result of immunization with a
vaccine. The internal structural proteins are not believed to be
involved in humoral or cell-mediated immunity.
ADEPT
Abbreviation for antibody-directed enzyme/pro-drug
therapy. Treatment for cancer in which an immunoconjugate
comprised of monoclonal antibody is united with an
enzyme with the capacity to transform an inert pro-drug
into an active cytotoxic drug.
adherent cell
A cell such as a macrophage (mononuclear phagocyte) that
attaches to the wall of a culture flask, thereby facilitating
the separation of such cells from B and T lymphocytes that
are not adherent.
adhesins
Bacterial products that split proteins. They combine with
human epithelial cell glycoprotein or glycolipid receptors,
which may account for the increased incidence of pulmonary
involvement attributable to Pseudomonas aeruginosa
in patients who are intubated.
adhesion molecule
Molecules that mediate cell adhesion to their surroundings
and to neighboring cells. In the immune system, adhesion
molecules are critical to most aspects of leukocyte function,
including lymphocyte recirculation through lymphoid
organs, leukocyte recruitment into inflammatory sites,
antigen-specific recognition, and wound healing. The five
principal structural families of adhesion molecules are
(1) integrins, (2) immunoglobulin superfamily (IgSF) proteins,
(3) selectins, (4) mucins, and (5) cadherins.
adhesion molecule assays
Cell adhesion molecules are cell surface proteins involved
in the binding of cells to each other, to endothelial cells,
or to the extracellular matrix. Specific signals produced in
response to wounding and infection control the expression
and activation of the adhesion molecule. The interactions
and responses initiated by the binding of these adhesion
molecules to their receptors and ligands play important roles
in the mediation of the inflammatory and immune reactions.
adhesion proteins
Extracellular matrix proteins that attract leukocytes from
the circulation. For example, T and B lymphocytes possess
lymph node homing receptors on their membranes that
facilitate their passage through high endothelial venules.
Neutrophils migrate to areas of inflammation in response to
endothelial leukocyte adhesion molecule 1 (ELAM-1) stimulated
by tumor necrosis factor (TNF) and interleukin-1 (IL-1)
on the endothelia of vessels. B and T lymphocytes that pass
A