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graft-vs.-leukemia (GVL) 302 granulocyte colony-stimulating factor (g-CSF)
donor and recipient, (2) passively transferred immunologically
reactive cells, and (3) a recipient host who has been
either naturally immunosuppressed because of immaturity
or genetic defect or deliberately immunosuppressed by
irradiation or drugs. The immunocompetent grafted cells
are especially reactive against rapidly dividing cells. Target
organs include the skin, gastrointestinal tract (including
the gastric mucosa), liver, and lymphoid tissues. Patients
often develop skin rashes and hepatosplenomegaly and may
have aplasia of the bone marrow. GVHR usually develops
within 7 to 30 days following the transplant or infusion of
the lymphocytes. Prevention of the GVHR is an important
procedural step in several forms of transplantation and may
be accomplished by irradiating the transplant. The clinical
course of GVHR may take a hyperacute, acute, or chronic
form, as seen in graft rejection.
graft-vs.-leukemia (GVL)
Bone marrow or stem cell transplantation as therapy for
leukemia. Partial genetic incompatibility between donor
and recipient is believed to facilitate elimination of residual
leukemia cells by NK cells and T lymphocytes from the
allogeneic transplant. This is a very desirable consequence
of MiHA and MHC mismatches between recipient and
donor. Also termed graft-vs.-tumor effect.
Gram-negative bacteria
Microorganisms with thin cell walls that contain peptidoglycan
and lipopolysaccharide (LPS) that stain red in the
Gram staining technique.
Gram-positive bacteria
Microorganisms with thick cell walls that contain peptidoglycan
and lipotechoic and techoic acids that stain purple in
the Gram staining technique.
granular cells
Hemocytes that express PRR in higher invertebrates that
facilitate wound healing and coagulation to entrap pathogenic
microorganisms. They also synthesize bactericidal
proteins and opsonins that aid encapsulation by phagocytic
cells. Also termed hemostatic cells.
granule exocytosis pathway
A mechanism used by armed cytotoxic T lymphocytes
(CTLs) to kill target cells. Following conjugate formation
and T cell receptor activation, the CTL repositions its Golgi
apparatus, permitting its preformed cytotoxic granules
to fuse with the CTL membrane. The granule contents,
comprised of perforin and granzymes, are exocytosed in the
direction of the target cell membrane, which leads to target
cell apoptosis.
granulocyte antibodies
Immunoglobulin G (IgG) and/or IgM antibodies present
in approximately 33% of adult patients with idiopathic
neutropenia. They are also implicated in the pathogenesis
of drug-induced neutropenia, febrile transfusion reactions,
isoimmune neonatal neutropenia, Evans syndrome, primary
autoimmune neutropenia of early childhood, systemic lupus
erythematosus, Graves’ disease, the neutropenia of Felty
syndrome and selected other autoimmune diseases.
granulocyte autoantibodies
Autoantibodies against granulocytes that serve as the
principal cause of autoimmune neutropenia (AIN).
Autoantibodies to the neutrophil-specific antigens of the
NA system are associated with this condition. Fifty percent
of patients with systemic lupus erythematosus (SLE) have
granulocyte autoantibodies, which are also found in febrile,
non-hemolytic transfusion reactions, transfusion-associated
acute lung injury, and alloimmune neonatal neutropenia
(ANN). Granulocyte autoantibodies on the neutrophil
surface can be detected by immunofluorescence (GIFT),
enzyme immunoassay (EIA), radioimmunoassay (RIA), or
flow cytometry (FC) or indirectly by detection of autoantibody
effects. Granulocyte autoantibodies are mainly of the
IgG isotype. Flow cytometry is preferred for assay of these
autoantibodies.
granulocyte chemotactic protein-2 (GCP-2)
A chemokine of the α family (CXC family). Osteosarcoma
cells can produce both human GCP-2 and interleukin-8
(IL8). The bovine homolog of human CP-2 has been demonstrated
in kidney tumor cells. Human and bovine GCP-2
are chemotactic for human granulocytes and activate postreceptor
mechanisms that cause the release of gelatinase B,
which portends a possible role in inflammation and tumor
cell invasion. Tissue sources include osteosarcoma cells and
kidney neoplastic cells. Granulocytes are the target cells.
Cys
74
Cys
64
NH 2
COOH
Granulocyte colony-stimulating factor (g-CSF).
Cys
42
granulocyte colony-stimulating factor (g-CSF)
A cytokine synthesized by activated T lymphocytes, macrophages,
and endothelial cells at infection sites that causes
bone marrow to increase the production and mobilization
Cys
36