| First Author | Collins BE | Year | 2006 |
| Journal | Nat Immunol | Volume | 7 |
| Issue | 2 | Pages | 199-206 |
| PubMed ID | 16369536 | Mgi Jnum | J:112390 |
| Mgi Id | MGI:3656192 | Doi | 10.1038/ni1283 |
| Citation | Collins BE, et al. (2006) Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling. Nat Immunol 7(2):199-206 |
| abstractText | CD22 is a negative regulator of B cell signaling, an activity modulated by its interaction with glycan ligands containing alpha2-6-linked sialic acids. B cells deficient in the enzyme (ST6Gal I) that forms the CD22 ligand show suppressed BCR signaling. Here we report that mice deficient in both CD22 and its ligand (Cd22-/- St6gal1-/- mice) showed restored B cell receptor (BCR) signaling, suggesting that the suppressed signaling of St6gal1-/- cells is mediated through CD22. Coincident with suppressed BCR signaling, B cells lacking ST6Gal I showed a net redistribution of the BCR to clathrin-rich microdomains containing most of the CD22, resulting in a twofold increase in the localization of CD22 together with the BCR. These studies suggest an important function for the CD22-ligand interaction in regulating BCR signaling and microdomain localization. |
