| First Author | Bischof D | Year | 2006 |
| Journal | Blood | Volume | 107 |
| Issue | 8 | Pages | 3235-42 |
| PubMed ID | 16357320 | Mgi Jnum | J:131234 |
| Mgi Id | MGI:3773381 | Doi | 10.1182/blood-2005-01-0256 |
| Citation | Bischof D, et al. (2006) Selective activation of TACI by syndecan-2. Blood 107(8):3235-42 |
| abstractText | 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. |
