The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/4/1355/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 8, April 20, 1998 1355-1360

Brief Definitive Reports

Requirement of SH2-containing Protein Tyrosine Phosphatases SHP-1 and SHP-2 for Paired Immunoglobulin-like Receptor B (PIR-B)–mediated Inhibitory Signal

Akito Maeda*, Mari Kurosaki*, Masao Ono{ddagger},§, Toshiyuki Takai{ddagger},§, and Tomohiro Kurosaki*

From the * Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the {ddagger} Department of Molecular Embryology, Institute of Development, Aging and Cancer, Tohoku University, Seiryo 4-1, Sendai 980-77, Japan; and § Core Research for Evolution Science and Technology, Japan Science and Technology Corporation, Japan

Paired immunoglobulin-like receptor B (PIR-B) (p91) molecule has been proposed to function as an inhibitory receptor in B cells and myeloid lineage cells. We demonstrate here that the cytoplasmic region of PIR-B is capable of inhibiting B cell activation. Mutational analysis of five cytoplasmic tyrosines indicate that tyrosine 771 in the motif VxYxxL plays the most crucial role in mediating the inhibitory signal. PIR-B–mediated inhibition was markedly reduced in the SH2-containing protein tyrosine phosphatases SHP-1 and SHP-2 double-deficient DT40 B cells, whereas this inhibition was unaffected in the inositol polyphosphate 5'-phosphatase SHIP-deficient cells. These data demonstrate that PIR-B can negatively regulate B cell receptor activation and that this PIR-B–mediated inhibition requires redundant functions of SHP-1 and SHP-2.

Address correspondence to Tomohiro Kurosaki, Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan. Phone: 81-6-993-9445; Fax: 81-6-994-6099; E-mail: kurosaki{at}mxr.meshnet.or.jp

We would like to acknowledge Dr. J.N. Ihle for providing us with the mouse SHP-1 cDNA.


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