| Literature DB >> 11828373 |
Tatjana Samardzic1, Dragan Marinkovic, Claus-Peter Danzer, Judith Gerlach, Lars Nitschke, Thomas Wirth.
Abstract
CD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.Entities:
Mesh:
Substances:
Year: 2002 PMID: 11828373 DOI: 10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H
Source DB: PubMed Journal: Eur J Immunol ISSN: 0014-2980 Impact factor: 5.532