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Blood, 15 April 2006, Vol. 107, No. 8, pp. 3235-3242.
Prepublished online as a Blood First Edition Paper on December 15, 2005; DOI 10.1182/blood-2005-01-0256.
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IMMUNOBIOLOGY
Selective activation of TACI by syndecan-2
Daniela Bischof,
Sherine F. Elsawa,
George Mantchev,
Juhan Yoon,
Grace E. Michels,
Allan Nilson,
Shari L. Sutor,
Jeffrey L. Platt,
Stephen M. Ansell,
Gotz von Bulow, and
Richard J. Bram
From the Departments of Pediatric and Adolescent Medicine, Immunology, Transplantation, and Hematology, Mayo Medical School, Mayo Clinic, Rochester, MN; and the Department of Microbiology and Immunology, the Department of Urology, and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis.
B-lymphocyte homeostasis and function are regulated by complementary actions of the TNFR family members TACI, BCMA, and BAFF-R, which are expressed by mature B cells. How these receptors are differentially activated is not entirely understood, because the primary ligand BAFF binds to all three. We searched for alternative ligands for TACI using recombinant TACI-Fc fusion protein as a probe and identified syndecan-2 as a new binding partner. TACI binding appears to require heparan sulfate posttranslational modifications of syndecan-2, because free heparin or pretreatment with heparitinase blocked the interaction. Syndecan-2 bound TACI but bound neither BAFF-R nor BCMA. Transfected cells expressing syndecan-2 activated signaling through TACI, as indicated by an NFAT-specific reporter. Syndecan-1 and syndecan-4 were also able to induce TACI signaling in a similar manner. This is the first identification of ligands that selectively activate TACI without simultaneously triggering BCMA or BAFF-R. This finding may help explain the alternative outcomes of signaling from this family of receptors in B cells.
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