Nature Immunology 7, 199 - 206 (2005)
Published online: 20 December 2005; | doi:10.1038/ni1283
Ablation of CD22 in ligand-deficient mice restores B cell receptor signalingBrian E Collins1, 4, Brian A Smith2, 4, Per Bengtson1, 3
& James C Paulson11
Departments of Molecular Biology and Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. 2
Sidney Kimmel Cancer Center, La Jolla, California 92037, USA. 3
Present address: Department of Clinical Science, Division of Oncology, Lund University, 22185 Lund, Sweden. 4
These authors contributed equally to this work.
Correspondence should be addressed to James C Paulson jpaulson@scripps.edu CD22 is a negative regulator of B cell signaling, an activity modulated by its interaction with glycan ligands containing  2-6-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.
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