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endoplasmic reticulum autoantibodies 248 endotoxin
endoplasmic reticulum. Selected membrane and organelle
proteins and secreted proteins are synthesized in the rough
endoplasmic reticulum. Cells such as plasma cells that
produce antibodies or other specialized secretory proteins
have abundant rough endoplasmic reticulum in the cytoplasm.
Following formation, proteins move from the rough
endoplasmic reticulum to the Golgi complex. They may
be transported in vesicles that form from the endoplasmic
reticulum and fuse with Golgi complex membranes. Once
secreted protein reaches the endoplasmic reticulum lumen,
it does not have to cross any further barriers prior to exit
from the cell.
endoplasmic reticulum autoantibodies
Autoantibodies against trifluoroacetylated (TFA) hepatic
proteins in patients who have developed a severe form of
halothane-induced hepatitis alluded to be induced by an
immune response. The sera of these patients also contain
antibodies that recognize various non-TFA-modified proteins
that may be present in patients who have been exposed
to halothane but do not develop hepatitis. Halothane anesthetic
can lead to mild halothane-induced liver damage that
is of no clinical significance or can cause the severe form.
The clinical significance of antibodies to TNA and non-
TFA proteins remains to be determined.
endorphin
An endogenous opioid peptide that links to a cognate receptor;
α, β, and γ types exist. The β endorphin is associated
with secretion by the pituitary gland and is possibly associated
with pain perception.
endosome
A 0.1- to 0.2-μm intracellular vesicle produced by endocytosis.
Extracellular proteins are internalized in this structure
during antigen processing. The endosome has an acidic pH
and contains proteolytic enzymes that degrade proteins
into peptides that bind to major histocompatibility complex
(MHC) class II molecules. MIICs, a subset of MHC-class-
II-rich endosomes, play a critical role in antigen processing
and presentation by the class II pathway.
endothelial cell antibodies (ECAs)
Immunoglobulin G (IgG) antibodies present in the sera
of systemic lupus erythematosus (SLE) patients that
may mediate immunologic injury to blood vessel walls.
They may be involved in the pathogenesis of rheumatoid
vasculitis. Besides SLE, cytotoxic antibodies reactive with
vascular endothelial cells are present in the sera of cardiac
allograft recipients undergoing hyperacute rejection
despite negative cross matches. ECAs may also be found
in patients with hemolytic uremic syndrome, in Kawasaki
disease, and in renal allograft recipients who have rejected
transplants. Selected patients with Wegener’s granulomatosis
and with micropolyarteritis may reveal noncytolytic
ECAs that are also demonstrable in 44% of dermatomyositis
patients, particularly those who also have interstitial
lung disease. About 33% of IgA nephropathy patients
possess antibodies that show specificity for vascular
endothelial cells and for human leukocyte antigen (HLA)
class I antigens.
endothelial cell autoantibodies (ECAs)
A heterogeneous family of antibodies that react with
various antigens expressed on resting and activated
endothelial cells. Some are associated with nephritis in
systemic lupus erythematosus (SLE), but ECAs are not
SLE-restricted. Cytotoxic antibodies against vascular
endothelial cells have been demonstrated in subjects
with hyperacute rejection of cardiac allografts who have
had compatible direct lymphocytotoxic crossmatches,
in patients who rejected renal allografts, in hemolytic–
uremic syndrome, and in Kawasaki disease. ECAs that
are not cytolytic have been demonstrated in patients with
micropolyarteritis and Wegener’s granulomatosis and in
approximately 44% of dermatomyositis patients. Serum
antibodies that bind to vascular endothelial cells, some
with anti-HLA class I specificity, have been demonstrated
in about one third of patients with IgA nepropathy. Sera
from scleroderma, Wegener’s granulomatosis, and microscopic
polyarteritis patients mediate antibody-dependent
cellular cytoxicity. Cytokine-mediated activation of
vascular endothelium is believed to be significant in the
pathogenesis of antibody-mediated and cell-mediated
entry to blood vessels.
endothelial leukocyte adhesion molecule 1 (ELAM-1)
Facilitates focal adhesion of leukocyte to blood vessel walls.
It is induced by endotoxins and cytokines and belongs to the
adhesion molecule family. It is considered to play a significant
role in the pathogenesis of atherosclerosis and infectious
and autoimmune diseases. Neutrophil and monocyte
adherence to endothelial cells occurs during inflammation
in vivo, along with leukocyte margination and migration
to areas of inflammation. Endothelial cells activated by
interleukin-1 (IL1) and tumor necrosis factor (TNF) synthesize
ELAM-1, at least in culture. A 115-kDa chain and a
100-kDa chain comprise the ELAM-1 molecule.
endothelin
A peptide composed of 21 amino acid residues derived from
aortic endothelial cells that serves as a powerful vasoconstrictor.
A gene on chromosome 6 encodes the molecule. It
produces an extended pressor response, stimulates release
of aldosterone, inhibits release of renin, and impairs renal
excretion. It is elevated in myocardial infarction and
cardiogenic shock, major abdominal surgery, pulmonary
hypertension, and uremia. It may have a role in the development
of congestive heart failure.
endotoxin
A Gram-negative bacterial cell wall lipopolysaccharide
(LPS) that is heat stable and causes neutrophils to release
pyrogens. It may produce endotoxin or hemorrhagic shock
and modify resistance against infection. Endotoxins
comprise integral constituents of outer membranes of
Gram-negative microorganisms. They are significant
virulence factors and induce injury in a number of ways.
Toxicity is associated with the lipid A fraction of the
molecule composed of a β-1,6-glucosaminyl-glucosamine
disaccharide substituted with phosphate groups and fatty
acids. LPS has multiple biological properties including
the ability to induce fever, lethal action, initiation of both
complement and blood coagulation cascades, and mitogenic
effects on B lymphocytes. It has the ability to stimulate production
of such cytokines as tumor necrosis factor (TNF)
and interleukin-1 (IL1) and the ability to clot Limulus
amebocyte lysate. Cytokines induced by endotoxins cause
fever, increased capillary permeability, and possible endotoxic
shock. Relatively large amounts of LPS released from
Gram-negative bacteria during Gram-negative septicemia
may produce endotoxin shock.