Treatment with human GM-CSF also induced anti-leishmanial activity but with little effect on peripheral leukocyte number or tissue myelomonocytic cell influx; human G-CSF stimulated marked peripheral granulocytosis and neutrophil tissue accumulation but induced little antileishmanial effect.
The clones differed in morphology, growth characteristics, karyotype, production of G-CSF, histology of the tumors produced by inoculating the cultured cells, and in the development of granulocytosis in host mice transplanted with the cultured cells.
Chronic neutrophilic leukemia (CNL) is a rare BCR-ABL1-negative myeloid malignancy that is characterized by mature granulocytosis without dysgranulopoiesis.
JAK2V617F mutation screening is indicated for the evaluation of erythrocytosis, thrombocytosis, splanchnic vein thrombosis, and otherwise unexplained BCR-ABL1-negative granulocytosis.
Treatment with human GM-CSF also induced anti-leishmanial activity but with little effect on peripheral leukocyte number or tissue myelomonocytic cell influx; human G-CSF stimulated marked peripheral granulocytosis and neutrophil tissue accumulation but induced little antileishmanial effect.
In this study, we show that genetic ablation of Sema3E in mice results in increased lung granulocytosis, airway hyperresponsiveness, mucus overproduction, collagen deposition, and Th2/Th17 inflammation.
Considering genotype effects under conditions of immune stimulation, we observed suppressive effects of ADH1B*2 allele on leukocytosis (≥9,000/μl; 0.69 [0.50 to 0.97]), granulocytosis (≥6,500/μl; 0.66 [0.47 to 0.93]), and monocytosis (≥750/μl; 0.56 [0.39 to 0.79]).
Chronic neutrophilic leukemia (CNL) is a rare BCR-ABL1-negative myeloid malignancy that is characterized by mature granulocytosis without dysgranulopoiesis.
Here we demonstrate that mice lacking phospholipase Cδ1 develop granulocytosis associated with elevated serum levels of the granulopoietic cytokine interleukin-17.
These data suggest that erythrocytosis and granulocytosis in JAK2(V617F) mice are the net result of a complex interplay between cell intrinsic and extrinsic factors.
We conclude, first, that a chronic high level of TPO overexpression stimulates megakaryocytopoiesis and myelopoiesis leading to thrombocytosis and granulocytosis.
These data indicate that one mechanism by which Li may cause granulocytosis is through a transcriptional enhancement of TNF production and subsequent secretion by monocytes.
Features uniformly observed among each patient included recurrent, necrotic soft tissue infections, impaired pus formation, delayed wound healing, constant granulocytosis, severe abnormalities of adhesion-dependent granulocyte functions and a profound deficiency (3%-6% of normal) of Mac-1 glycoproteins on granulocyte surfaces.
Features uniformly observed among each patient included recurrent, necrotic soft tissue infections, impaired pus formation, delayed wound healing, constant granulocytosis, severe abnormalities of adhesion-dependent granulocyte functions and a profound deficiency (3%-6% of normal) of Mac-1 glycoproteins on granulocyte surfaces.