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J. Biol. Chem., Vol. 277, Issue 34, 30707-30715, August 23, 2002
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From the CD5+ B (or B-1) cells are the
normal precursors of B cell chronic lymphocytic leukemia. They
differ from conventional B (B-2) cells with respect to their phenotype
and mitogenic responses and are often secretors of the natural
polyreactive antibodies in the serum. The origin of B-1 cells remains
controversial, and the relationship between B-1 cells and autoreactive
B cells is unclear. Here, we compare the signaling pathways that are
activated by the engagement of the B cell antigen receptor (BCR) in B-1 and B-2 cells. Stimulation of the BCR leads to the induced activation of the three major classes of mitogen-activated protein kinases (MAPKs), ERK, JNK, and p38 MAPK, as well as the Akt kinase and the
transcription factors nuclear factor of activated T cells (NF-AT) and
NF-
Peritoneal CD5+ B-1 Cells Have Signaling Properties
Similar to Tolerant B Cells*
,,,, and¶
Institute of Molecular and Cell Biology, 30 Medical Dr., Singapore 117609, Singapore and the
§ Department of Physiology, Faculty of Medicine, National
University of Singapore, Singapore 117597, Singapore
B in B-2 cells. In contrast, B-1 cells have constitutive activation of ERK and NF-AT but exhibit delayed JNK and lack p38 MAPK
and NF-B induction upon BCR cross-linking. The lack of NF-B activation in B-1 cells may be due to a lack of Akt activation in these
cells. Furthermore, our study using specific inhibitors reveals that
the extended survival of B-1 cells in culture is not due to the
constitutive activation of ERK; nor is it due to Akt signaling or
Bcl-xL up-regulation, since these are not induced in B-1
cells. The current findings of altered MAPK and NF-AT activation and
lack of NF-B induction in B-1 cells indicate that these cells have
signaling properties similar to tolerant B cells that are chronically
exposed to self-antigens. Indeed, BCR stimulation of B-1 cells does not
lead to their full activation as indicated by their lack of maximal
up-regulation of specific markers such as CD25, CD69, and CD86.
*
This work is supported by grants from the Biomedical
Research Council of the Agency for Science, Technology, and Research.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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