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α 4 β 1 integrin‐mediated adhesion of CD34 + cells from patients with chronic myeloid leukaemia: influence of IL‐3
Author(s) -
Schofield K. P.,
Duerig J.,
Rushton G.,
Chang J.
Publication year - 1999
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1999.01583.x
Subject(s) - cd34 , fibronectin , integrin , haematopoiesis , progenitor cell , myeloid , adhesion , cell adhesion , stromal cell , cord blood , cell adhesion molecule , immunology , stem cell , microbiology and biotechnology , biology , chemistry , cancer research , cell , extracellular matrix , biochemistry , organic chemistry
Interactions between integrins on haemopoietic progenitor cells and their stromal ligands have an important role in the control of haemopoiesis. Growth factors can modulate these interactions (so‐called ‘inside‐out’ signalling) resulting in changes in ligand binding activity. We have studied α 4 β 1 integrin‐mediated adhesion to the H120 fragment of fibronectin (which contains the strongest α 4 β 1 binding site) in CD34 + cells from patients with chronic myeloid leukaemia (CML) and have determined the effect of IL‐3 on the level of adhesion. Compared to normal CD34 + cells isolated from cord blood and peripheral blood progenitor harvests (mean of 61.4 ± 14.9% of cells attached) the CML CD34 + cells showed reduced levels of adhesion (mean of 41.9 ± 14.7%, P < 0.05). The effect of 10 ng/ml of IL‐3 resulting in reduced adhesion of normal CD34 + cells at 30 min was absent in 6/7 patients with CML. Abnormalities of adhesion to fibronectin may thus be related to IL‐3 pathways affected by BCR‐ABL. These findings will have implications for understanding the dysregulation of growth and adhesion in CML.