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Bcl-2 proteins 103 Bence–Jones (B–J) proteins
the endosome induces a conformational change in diphtheria
toxin that triggers membrane insertion of the membranespanning
domains. Pore formation by dimerization is
thought to occur, and the toxic subunit diphtheria toxin is
translocated from the endosomal lumen into the cytosol. It
is clear from reconstitution assays that many members of
the Bcl-2 family can form a pore that allows passage of ions
or elicits the release of cytochrome c from isolated mitochondria.
Passage of ions is more dramatic at low pH. The
carboxyl mitochondria targeting sequence is not required
for in vitro pore formation.
Bcl-2 proteins
Proteins that regulate the rate at which apoptotic signaling
events initiate or amplify caspase activity. Bcl-2 alters the
apoptotic threshold of a cell rather than inhibiting a specific
step in programmed cell death. Cells that overexpress
Bcl-2 still carry out programmed cell death in response to
a wide spectrum of apoptotic initiators. The dose of the
initiator is greater than in the absence of Bcl-2. Several
Bcl-2-related proteins have been identified. Whereas
some Bcl-2 family members promote cell survival, others
enhance the sensitivity of a cell to programmed death.
Five homologs of Bcl-2 with antiapoptotic properties
include Bcl-x L, Bcl-w, Mcl-l, NR-13, and A-1. By contrast,
two proapoptotic members of the Bcl-2 family include Bax
and Bak. Bcl-2-related proteins are present in the intracellular
membranes, including the endoplasmic reticulum,
outer mitocondrial membrane, and outer nuclear membrane.
Bcl-2 proteins are hypothesized to regulate membrane
permeability.
Bcl-X L
A Bcl-2-related protein that is upregulated through the
action of the costimulatory molecules CD28 and CD40.
Bcl-X L expression is claimed to prevent cell death in
response to growth factor limitation or Fas signal transduction.
Signal transduction through CD28 or CD40 induces
Bcl-X L expression only in antigen-activated cells. Without
antigen–receptor engagement, CD40 engagement promotes
cell death. Bcl-x L induction by either CD28 or CD40 is transient,
persisting only 3 to 4 days. Protection of cells from
death lasts only as long as Bcl-x L is expressed.
BCR/cABL
Fusion gene that can be detected by either chromosomal
analysis or polymerase chain reaction (PCR)-based
molecular assays. There is also a total lack of leukocyte
alkaline phosphatase.
BDB
Refer to bis-diazotized benzidine.
Behçet’s disease
Oral and genital ulcers, vasculitis, and arthritis that recur as
a chronic disease in young men. It is postulated to have an
immunologic basis and possibly to be immune complex-mediated.
Perivascular infiltrates of lymphocytes may occur.
The serum contains immune complexes, and immunofluorescence
may reveal autoantibodies against the oral mucous
membrane. It is associated with HLA-1 in ethnic groups,
but not Caucasians. The principal immunologic dysfunction
in Behçet’s disease is neutrophil hyperfunction, shown
by augmented chemotactic responsiveness and superoxide
production. Behçet’s disease is an inflammatory condition
of uncertain cause. No autoimmune mechanism has been
proven.
Emil Adolph von Behring (1854–1917).
Emil Adolph von Behring with colleagues in the laboratory.
Behring, Emil Adolph von (1854–1917)
German bacteriologist who, with Kitasato, demonstrated
that circulating antitoxins against diphtheria and tetanus
conferred immunity. Received the first Nobel Prize for
Medicine in 1901 for this work. (Related works include
Die Blutserumtherapie, 1902; Gesammelte Abhandlungen,
1915; Behring, Gestalt und Werk, 1940; Emil von Behring
zum Gedachtnis, 1942.)
beige mice
A mutant strain of mice that develops abnormalities
in pigment, defects in natural killer cell function, and
heightened tumor incidence, serving as a model for the
Chediak–Higashi disease in humans. There is a defect in
granule function. The strain has also been used as an NK
cell-deficient murine model.
Benacerraf, Baruj (1920–)
American immunologist born in Caracas, Venezuela. His
multiple contributions include the carrier effect in delayedtype
hypersensitivity, lymphocyte subsets, major histocompatibility
complex (MHC), and Ir immunogenetics, for
which he received the Nobel Prize in 1980. (Benacerraf,
B. and Unanue, E., Textbook of Immunology, Williams &
Wilkins, Baltimore, Maryland, 1979.)
Bence–Jones (B–J) proteins
Represent the light chains of either the κ or λ variant
excreted in the urine of patients with a paraproteinemia as
B