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* Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01655; and
Rosenstiel Research Center and Department of Biology, Brandeis University, Waltham, MA 02254
Naive peripheral B cells are maintained in sufficient numbers and
diversity to mount effective immune responses against infectious
agents. However, the size and repertoire of this B cell pool is
constantly diminished by normal cell turnover and Ag activation.
Homeostatic (Ag-independent) proliferation in response to B cell
depletion is one mechanism to compensate for this cell loss. We have
used purified CFSE-labeled B cells and an adoptive transfer model
system to show that immature and mature B cells divide in a variety of
B cell-deficient (scid, xid,
IL-7-/-, and sublethally irradiated) hosts.
Homeostatic B cell proliferation is T cell independent, and B cells
that have replicated by this mechanism retain the antigenic phenotype
of naive B cells. Replication is significantly reduced in B
cell-sufficient normal or B cell-reconstituted immunodeficient
recipients by the action of competing mature follicular B cells. Using
xid mice and transcription factor knockouts, we show
that the activation signal(s) that lead to homeostatic B cell
proliferation require Bruton’s tyrosine kinase; however, c-Rel,
a Bruton’s tyrosine kinase-induced NF-
B/Rel transcription factor
critical for Ag and mitogen stimulation, is dispensable, indicating the
uniqueness of this activation pathway. Survival and replication signals
can also be separated, because the transcription factor p50 (NF-B1),
which is required for the survival of peripheral B cells, is not
necessary for homeostatic replication. Homeostatic B cell proliferation
provides an Ag-independent mechanism for the maintenance and expansion
of naive B cells selected into the mature B cell
pool.
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