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Antigen receptor nonresponsiveness in chronic lymphocytic leukemia B cells
AC Lankester, GM van Schijndel, CE van der Schoot, MH van Oers, CJ van Noesel and RA van Lier
Department of Clinical Viro-Immunology and Immunohematology, Central
Laboratory of the Netherlands Red Cross Blood Transfusion Service,
Amsterdam, The Netherlands.
B chronic lymphocytic leukemia (B-CLL) are clonal populations of mIgM+ or
mIgM+/mIgD+ CD5+ B cells that appear to be arrested in the follicular
mantle-zone B-cell stage. Functional analyses have shown two groups of
B-CLL that can be distinguished based on their capacity to proliferate in
response to B-cell antigen receptor complex (BCR) cross- linking. To
investigate the molecular basis for this phenomenon, we have analyzed both
architecture and functional properties of BCR complexes on these two groups
of B-CLL. Both groups were found to express structurally similar BCR.
However, protein tyrosine kinase (PTK) activity associated with and
specific for BCR constituents was strongly diminished in nonresponsive
B-CLL. Moreover, the PTK-dependent assembly of Shc/Grb2 complexes, which
may couple the BCR to p21ras, was absent in these B-CLL. Finally, of all
PTKs tested, the expression of PTK syk was found to be considerably lower
in nonresponsive B-CLL. Thus, absence of mitogenic responses upon BCR
cross-linking in particular B-CLL was found to be strictly correlated with
diminished induction of BCR-associated PTK activity and lower levels of PTK
syk. Because nonresponsive B-CLL closely resembles tolerant autoreactive B
cells both functionally and biochemically, distinction between B-CLL with
respect to functional properties in vitro may be determined by differences
in antigen encounter in vivo.
Volume 86,
Issue 3,
pp. 1090-1071,
08/01/1995
Copyright © 1995 by The American Society of Hematology
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