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.
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20 April 1998
Brief Definitive Report|
April 20 1998
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,
Akito Maeda
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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Mari Kurosaki,
Mari Kurosaki
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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Masao Ono,
Masao Ono
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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Toshiyuki Takai,
Toshiyuki Takai
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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Tomohiro Kurosaki
Tomohiro Kurosaki
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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Akito Maeda
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
Mari Kurosaki
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
Masao Ono
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
Toshiyuki Takai
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
Tomohiro Kurosaki
From the *Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan; the ‡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
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: [email protected]
We would like to acknowledge Dr. J.N. Ihle for providing us with the mouse SHP-1 cDNA.
Received:
December 08 1997
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1998
J Exp Med (1998) 187 (8): 1355–1360.
Article history
Received:
December 08 1997
Citation
Akito Maeda, Mari Kurosaki, Masao Ono, Toshiyuki Takai, Tomohiro Kurosaki; Requirement of SH2-containing Protein Tyrosine Phosphatases SHP-1 and SHP-2 for Paired Immunoglobulin-like Receptor B (PIR-B)–mediated Inhibitory Signal . J Exp Med 20 April 1998; 187 (8): 1355–1360. doi: https://doi.org/10.1084/jem.187.8.1355
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