CD22, a B lymphocyte-specific adhesion molecule that regulates antigen receptor signaling.

Journal Article (Journal Article;Review)

The development of B lymphocytes is a highly regulated process that depends in part on lineage-specific cell surface molecules. In addition, transmembrane signals generated through the B cell antigen receptor and other surface molecules regulate B cell responses to foreign antigens. Recent studies reveal CD22 to be a functionally significant receptor during these processes. CD22 is first expressed in the cytoplasm of pro-B and pre-B cells, and on the surface as B cells mature to become IgD+. CD22 is a member of the Ig superfamily that serves as an adhesion receptor for sialic acid-bearing ligands expressed on erythrocytes and all leukocyte classes. In addition to its potential role as a mediator of intercellular interactions, signal transduction through CD22 can activate B cells and modulate antigen receptor signaling in vitro. CD22 signaling is mediated via interactions with a number of kinases and phosphatases that bind the cytoplasmic domain through phosphorylated tyrosine residues located within consensus TAM and TIM motifs. The phenotype of CD22-deficient mice suggests that CD22 is primarily involved in the generation of mature B cells within the bone marrow, blood, and marginal zones of lymphoid tissues. Most notable in CD22-deficient mice is a significant diminution of surface Ig levels in these B cell subpopulations, which suggests that CD22 functions in vivo to adjust the signaling threshold of cell surface antigen receptors. A further understanding of CD22 function is required and may reveal roles for CD22 in disease susceptibility or the development of autoimmunity.

Full Text

Duke Authors

Cited Authors

  • Tedder, TF; Tuscano, J; Sato, S; Kehrl, JH

Published Date

  • 1997

Published In

Volume / Issue

  • 15 /

Start / End Page

  • 481 - 504

PubMed ID

  • 9143697

International Standard Serial Number (ISSN)

  • 0732-0582

Digital Object Identifier (DOI)

  • 10.1146/annurev.immunol.15.1.481


  • eng

Conference Location

  • United States