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J Biol Chem, Vol. 275, Issue 1, 548-556, January 7, 2000
From the Genetic studies revealed that CD5 could be a
negative regulator of the B-cell antigen receptor (BCR). We explore
here the effect of human CD5 on BCR-triggered responses. B cells were
obtained expressing a chimera composed of extracellular and
transmembrane domains of Fc
The Pseudo-immunoreceptor Tyrosine-based Activation Motif of CD5
Mediates Its Inhibitory Action on B-cell Receptor Signaling*
,,,
Laboratoire d'Immunologie Cellulaire, CNRS
UMR 7627, Centre Hospitalier Pitié-Salpêtrière,
CERVI, 83 Boulevard de l'Hôpital, 75013 Paris, France and the
§ Laboratoire d'Immunologie Cellulaire et Clinique, INSERM
U255, Institut Curie, 26 rue d'Ulm, 75005 Paris, France
type IIB receptor fused to CD5
cytoplasmic domain (CD5cyt). Coligation of the chimera with the BCR
induces CD5cyt tyrosine phosphorylation. A rapid inhibition of
BCR-induced calcium response is observed, as well as a partial but
delayed inhibition of phospholipase C-1 phosphorylation. Activation
of extracellular regulated kinase-2 is also severely impaired.
Moreover, at the functional level, interleukin-2 production is
abolished. Src homology 2 domain-bearing tyrosine phosphatase SHP-1 and
Src homology 2 domain-bearing inositol 5'-phosphatase SHIP usually
participate in negative regulation of the BCR. We show that they do not
associate with the phosphorylated CD5 chimera. We finally demonstrate
that the pseudo-immunoreceptor tyrosine based activation motif present in CD5cyt is involved because its deletion eliminates the inhibitory effect of the chimera, both at biochemical and functional levels. These
results demonstrate the inhibitory role of CD5 pseudo-immunoreceptor tyrosine based activation motif tyrosine phosphorylation on BCR signaling. They further support the idea that CD5 uses mechanisms different from those already described to negatively regulate the BCR pathway.
*
This work was supported by grants from the Association de la
Recherche sur le Cancer and the Ligue Nationale contre le Cancer.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.
To whom correspondence should be addressed: CNRS UMR 7627, Centre Hospitalier Pitié-Salpêtrière/CERVI, 83 Blvd
de l'Hôpital, 75013, Paris, France. Tel.: 33-1-42177489; Fax:
33-1-42177490; E-mail: gbismuth@ ccr.jussieu.fr.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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