Untitled - D Ank Unlimited

glucocorticoids (GCs) 296 Gm allotype
disease (membranoproliferative glomerulonephritis type
II), C3 alone is demonstrable in the dense deposits within
capillary walls. The types of primary glomerulonephritis
include acute diffuse proliferative GN, rapidly progressive
(crescentic) GN, membranous GN, lipoid nephrosis, focal
segmental glomerulosclerosis, membranoproliferative GN,
IgA nephropathy, and chronic GN. Secondary diseases
affecting the glomeruli include SLE, diabetes mellitus,
amyloidosis, Goodpasture’s syndrome, polyarteritis nodosa,
Wegener’s granulomatosis, Henoch–Schönlein purpura, and
bacterial endocarditis.
glucocorticoids (GCs)
Glucocorticoids are powerful immunosuppressive and
antiinflammatory drugs that have lympholytic properties.
They reduce circulating lymphocytes and monocytes,
in addition to suppressing interleukin-1 (IL1) and IL2
production. Glucocorticoid administration diminishes the
size and lymphoid content of the lymph nodes and spleen.
Glucocorticoids are cytotoxic to selected T cell subsets,
but their immunologic effects are probably attributable
to their capacity to modify cellular functions rather than
to direct cytotoxicity. Cellular immunity is affected more
than is humoral immunity. Continuous administration
increases the fractional catabolic rate of IgG, the principal
class of antibody immunoglobulin. Glucocorticoid
therapy usually abrogates DTH T cell-mediated contact
hypersensitivity. However, chronic use produces adverse
effects, including increased susceptibility to infection,
bone fractures, diabetes, and cataracts. GCs act by binding
to cytoplasmic GC receptor that regulates transcription
of cytokine genes associated with inflammation. GCs
regulate expression of the cytokines TNF-α, granulocyte–
macrophage colony-stimulating factor (GC-CSF), IL1,
IL2, IL3, IL4, IL5, IL6, and IL8. IL1, IL6, and TNF-α
induce GC release in a prostaglandin–corticotropin-releasing,
hormone-dependent manner from the hypothalamic–
pituitary–adrenal axis. GCs are powerful inhibitors of
nitric oxide synthase induction and induce the expression
of the 37-kDa immunomodulator, lipocortin-1, in PMNLs
and macrophages. Lipocortin is a powerful inhibitor of
phospholipase A 2, which releases arachidonic acid for
proinflammatory eicosanoid synthesis. GCs downregulate
expression of the eosinophil chemokine RANTES.
Endogenous GCs (corticosterone) inhibit neutrophil
chemotaxis in inflammatory cholestasis. GCs also induce
a prolonged increase in plasma cortisol.
glucose-6-phosphate dehydrogenase deficiency
Occasionally, individuals of both sexes have been shown
to have no glucose-6-phosphate dehydrogenase in their
leukocytes. This could be associated with deficient NADPH
with diminished hexose monophosphate shunt activity
and reduced formation of hydrogen peroxide in leukocytes,
which are unable to kill microorganisms intracellularly,
as described in chronic granulomatous disease
(CGD). Clinical aspects resemble those in CGD, except
that glucose-6-phosphate dehydrogenase deficiency occurs
later and affects both sexes, in addition to being associated
with hemolytic anemia. Although the nitroblue tetrazolium
(NBT) test is within normal limits, glucose-6-phosphate
dehydrogenase activity is deficient, the killing curve is
altered, formation of H 2O 2 is abnormal, and oxygen consumption
is inadequate. No effective treatment is available.
glutamic acid decarboxylase autoantibodies (GADs)
Autoantibodies associated with a rare neurological disorder
known as stiff man syndrome (SMS) and with insulindependent
diabetes mellitus (IDDM). Autoantibodies in the
sera of SMS patients react with denatured GADs on immunoblots.
By contrast, antibodies in IDDM patients react only
with native (nondenatured) GADs by immunoprecipitation.
In SMS, the frequency of GAD autoantibodies ranges from
60 to 100%; in IDDM, the frequency ranges from 25 to
79%. GAD autoantibodies are almost always present with
islet cell antibodies (ICA) and may represent a constituent
of ICA.
gluten-sensitive enteropathy (celiac sprue,
nontropical sprue)
A disease that results from defective gastrointestinal
absorption due to hypersensitivity to cereal grain storage
proteins, including gluten or its product gliadin, present in
wheat, barley, and oats. Diarrhea, weight loss, and steatorrhea
occur. It is characterized by villous atrophy and
malabsorption in the small intestine. It occurs mostly in
Caucasians and occasionally in African-Americans, but
not in Asians, and is associated with HLA-DR3 and DR7.
The disease may be limited to the intestines or associated
with dermatitis herpetiformis, a vesicular skin eruption.
Antigliadin antibodies which are immunoglobulin A (IgA)
are formed, and lymphocytes and plasma cells appear in
the lamina propria in association with villous atrophy.
Diagnosis is made by showing villous atrophy in a small
intestinal biopsy. Administering a gluten-free diet leads to
resolution of the disease.
GlyCAM-1
A vascular addressin molecule resembling mucin that is
present on high endothelial venules in lymphoid tissues.
L-selectin molecules on lymphocytes in the peripheral
blood bind GlyCAM-1 molecules, causing the lymphocytes
to exit the blood circulation and enter the lymphoid tissues.
glycocalyx
A thick layer of mucin-like molecules in the apical membranes
of the brush borders of intestinal epithelial cells. It
possesses hydrolytic enzymes and has a negative charge
that repels pathogenic microorganisms.
glycosyl phosphatidylinositol (GPI)-linked
membrane antigens
A class of cell surface antigens attached to membranes
by glycosyl phosphatidylinositol. Monoclonal antibody
studies indicate that in both human and murine subjects
GTI-linked antigens are capable of stimulating T cells and
sometimes B cells. Structurally, they are diverse. See also
Ly-5 and Qa-2.
Gm allotype
A genetic variant determinant of the human immunoglobulin
G (IgG) heavy chain. Allelic genes that encode the γ1,
γ2, and γ3 heavy chain constant regions encode the Gm
allotypes. They were recognized by the ability of sera from
rheumatoid arthritis patients containing anti-IgG rheumatoid
factor to react with them. Gm allotypic determinants
are associated with specific amino acid substitution in
different γ chain constant regions in humans. IgG subclasses
are associated with certain Gm determinants. For
example, IgG 1 is associated with G 1m(1) and G 1m(4), and
IgG 3 is associated with G 3m(5). Although the majority of
Gm allotypes are restricted to the IgG-γ chain Fc region,