
Differential adhesion pattern of B cell chronic lymphocytic leukemia cells
Author(s) -
S. Behr,
Dirk Korinth,
Folke Schriever
Publication year - 1998
Publication title -
leukemia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.539
H-Index - 192
eISSN - 1476-5551
pISSN - 0887-6924
DOI - 10.1038/sj.leu.2400883
Subject(s) - chronic lymphocytic leukemia , cell adhesion molecule , cell adhesion , cd19 , neural cell adhesion molecule , germinal center , microbiology and biotechnology , biology , integrin , b cell , adhesion , immunology , chemistry , leukemia , antibody , cell , biochemistry , organic chemistry
Binding of B cell chronic lymphocytic leukemia (B-CLL) cells to other cells and to extracellular matrices influences the pathophysiology and the clinical presentation of the B-CLL disease. It is still unknown which adhesion pathways regulate the traffic of B-CLL cells within distinct histologic compartments of lymphoid organs. In addition, it is not yet clarified which mechanisms mediate the intercellular adhesion of B-CLL cells. The present study sought to identify the mechanisms that are involved in the binding of B-CLL cells to secondary lymphoid organs in situ and in the homotypic aggregation of these cells. B-CLL cells specifically bound to germinal centers of normal human tonsils via the adhesion pair integrin alpha4beta1/vascular cell adhesion molecule-1 (VCAM-1). Among a large panel of antibodies tested only mAbs against CD19 induced homotypic adhesion of B-CLL cells via the adhesion molecules integrin alphaL (leukocyte function antigen-1 (LFA-1)), intercellular adhesion molecule-1 (ICAM-1) and CD21. Anti-CD19-induced aggregation required protein synthesis. We hypothesize that the observed heterotypic and homotypic adhesion of B-CLL cells reflects the ability of these leukemic cells to migrate in vivo.