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Nat Immunol. 2006 Feb;7(2):199-206. Epub 2005 Dec 20.

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

Author information

1
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.

Abstract

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.

PMID:
16369536
DOI:
10.1038/ni1283
[Indexed for MEDLINE]

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