International Immunology, Vol 10, 141-146, Copyright © 1998 by Oxford University Press
G Koncz, J Gergely and G Sarmay
Fc gammaRIIb (CD32) controls antibody production by down-regulating cell
activation, when co-clustered with B cell antigen receptors (BCR) in vivo,
via immune complexes consisting of secreted IgG and antigen. Fc
gammaRIIb-BCR co-ligation in vitro was shown to inhibit the Ca2+ influx
from the extracellular space, the mechanism of which is not fully
understood. Human B cells express Fc gammaRIIb1 and Fc gammaRIIb2,
differing only in a 19 amino acid long insert in the cytoplasmic tail of
the former. To elucidate whether Fc gammaRIIb1 and Fc gammaRIIb2 isoforms
show any difference in the down-regulation of B cells, we have studied the
effect of co-clustering of BCR and Fc gammaRIIb1 or Fc gammaRIIb2 on the
Ca2+ signaling in a Burkitt's lymphoma cell line, ST486, transfected with
the two isoforms respectively. We have shown here, for the first time, that
co- aggregation of BCR and Fc gammaRIIb may also inhibit Ca2+ release from
the endoplasmic reticulum pool of human B cells. Both isoforms mediated
this inhibition and the inhibitory effect depended on the ratio of BCR to
Fc gammaRIIb cross-linking. In contrast to Fc gammaRIIb, the CD21/CD19
complex was shown to up-regulate B cell response by lowering the activation
threshold. We have shown here that co-clustering of Fc gammaRIIb with CD19
inhibited the CD19-induced Ca2+ influx. Furthermore, the three party
co-aggregation of Fc gammaRIIb with BCR and CD19 resulted in a decreased
Ca2+ response, as compared to the BCR- plus CD19-induced one, indicating
that Fc gammaRIIb may inhibit CD19- induced enhancement of B cell
activation. On the basis of these data we suggest that IgG-containing and
C3d-fixing immune complexes may down- regulate the B cell response by
interfering with both BCR- and CD19- mediated Ca2+ mobilization.
ARTICLES
Fc gammaRIIb inhibits both B cell receptor- and CD19-induced Ca2+ mobilization in Fc gammaR-transfected human B cells
Department of Immunology, Lorand Eotvos University, God, Hungary.
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