Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from two patients with granulocytopenia associated with collagen vascular disease caused the destruction of normal human granulocytes by autologous lymphocytes in vitro. Granulocyte cytotoxicity was measured by the release of 51Cr during incubation with test sera and lymphocytes in microtiter plates. Between 8% and 46% granulocytoxicity was produced in granulocytes from 8 normal donors by the sera from these two patients. Less than 6% granulocytotoxicity was seen with the sera from 14 normal subjects and 29 patient controls. Treatment of lymphocyte preparations with carbonyl iron and magnetic separation to remove phagocytic cells or treatment with complement-coated red cells followed by repeated gradient centrifugation to remove complement receptor-bearing lymphocytes did not reduce the granulocytotoxicity. There was a dose-response relationship between the concentration of positive sera and granulocytotoxicity. When these sera were fractionated by Sephadex G-200 gel filtration and by ion-exchange chromatography with DEAE-cellulose, the active component appeared in the IgG-containing fractions. Thus, IgG antibody-dependent, lymphocyte-mediated granulocyte cytotoxicity represents a means of detecting human granulocyte antibodies and is a possible mechanism of autoimmune neutropenia in these two patients.
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PMID:Antibody-dependent lymphocyte-mediated granulocyte cytotoxicity in man. 61 59

Colony-stimulating factor (CSF) was partially purified from urine of patients with aplastic anemia using DEAE-cellulose and concanavalin A-Sepharose. This partially purified CSF caused significant neutrophilia in the peripheral blood of normal mice by (a) single or continual intraperitoneal injection(s) in vivo, and also revealed a specific activity of 1.4 x 10(3) U/absorbance unit (AU) at 280 nm in vitro, with less than 1 ng/AU endotoxin. In addition, this CSF induced faster recoveries of neutrophils in the peripheral blood and progenitor spleen cells of cyclophosphamide (CY)-treated mice. These findings suggest that the CSF used in this study accelerated the differentiation of the granulocytic cells and the proliferation of granulocyte colony-forming units in the spleen. These effects contributed to a rapid recovery from neutropenia in mice treated with CY.
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PMID:Granulopoietic effects of colony-stimulating factor obtained from urine of patients with aplastic anemia on normal and cyclophosphamide-treated mice. 313 86