Soluble complement receptor 1 is increased in patients with leukemia and after administration of granulocyte colony-stimulating factor
Autor: | Sybille Schwarz, Olivier Spertini, Salima Sadallah, Alois Gratwohl, Estelle Lach, J A Schifferli |
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Rok vydání: | 1999 |
Předmět: |
Complement receptor 1
Chronic lymphocytic leukemia Immunology Enzyme-Linked Immunosorbent Assay Granulocyte Complement Receptor Type 1 hemic and lymphatic diseases Granulocyte macrophage colony-stimulating factor receptor Granulocyte Colony-Stimulating Factor medicine Animals Humans Immunology and Allergy L-Selectin Retrospective Studies biology Hematopoietic Stem Cell Transplantation Myeloid leukemia Complement System Proteins Cell Biology medicine.disease Tissue Donors Leukemia Lymphoid Leukemia medicine.anatomical_structure Solubility Leukemia Myeloid Receptors Complement 3b Rabbits biology.gene Granulocyte colony-stimulating factor receptor |
Zdroj: | Journal of Leukocyte Biology. 65:94-101 |
ISSN: | 1938-3673 0741-5400 |
Popis: | Complement receptor type 1 is expressed by erythrocytes and most leukocytes. A soluble form is shed from the leukocytes and found in plasma (sCR1). sCR1 is a powerful inhibitor of complement. We report an increased sCR1 in the plasma of leukemia patients, up to levels producing measurable complement inhibition. Half of the 180 patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic lymphocytic leukemia (CLL) had sCR1 levels above the normal range. The highest levels were observed in T-ALL (17 patients). The complement function of a T-ALL serum was improved by blocking sCR1 with a specific mAb (3D9). Measurements in 16 peripheral stem cell donors before and after granulocyte colony-stimulating factor (G-CSF) administration showed an increase in sCR1 (before, 43.8 ± 15.4; at day 5, 118.3 ± 44.7 ng/mL; P < 0.0001). This increase paralleled the increase in total leukocyte counts and was concomitant with de novo leukocyte mRNA CR1 expression in all three individuals tested. Whether pharmacological intervention may be used to up-regulate sCR1 so as to inhibit complement in vivo should be further investigated. J. Leukoc. Biol. 65: 94–101; 1999. |
Databáze: | OpenAIRE |
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