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Soluble complement receptor 1 is increased in patients with leukemia and after administration of granulocyte colony‐stimulating factor
Author(s) -
Sadallah Salima,
Lach Estelle,
Schwarz Sybille,
Gratwohl Alois,
Spertini Olivier,
Schifferli JürgAlfred
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.65.1.94
Subject(s) - complement receptor 1 , myeloid leukemia , biology , immunology , complement system , leukemia , granulocyte , complement receptor , acute lymphocytic leukemia , receptor , concomitant , medicine , antibody , lymphoblastic leukemia , biochemistry
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.