Engagement of the adhesion receptor cd22 triggers a potent stimulatory signal for b cells and blocking cd22/cd22l interactions impairs t-cell proliferation

Joseph Tuscano, T. F. Tedder, J. H. Kehrl

Research output: Contribution to journalArticle

Abstract

The B lymphocyte-restricted adhesion protein CD22 mediates sialic aciddependent cell-cell interactions. Engagement of CD22 on B lymphocytes with a CD22 mAb HB22.7 that blocks the binding of CD22 to its ligand(s) directly stimulated B-cell proliferation. In addition, the HB22.7 mAb co-stimulated B cell proliferation with either anti-lgM, interleukin (ID-2, IL-4, or CD40 and triggered predominantly B cell IgG secretion with IL-2. Even more striking levels of B cell proliferation occurred with HB22.7 mAb under culture conditions that enhanced B-B cell interactions. In contrast, a non-blocking CD22 mAb (CD22.5) poorly co-stimulated in similar experiments. The functional differences between the two antibodies likely result from differing abilities to trigger downstream signaling events as significant differences in CD22 tyrosine phosphorylation and the recruitment of the tyrosine kinase p53/56lyn and the tyrosine phosphatase SH-PTP1C were found. Besides their role in B cell stimulation, CD22/CD22L interactions may also assist in regulating T-cell proliferation because inhibition of CD22-CD22L engagement with the HB22.7 mAb impaired T cell proliferation in a co-stimulatory assay. Thus, CD22/CD22L interactions result in stimulatory signals for both B and T lymphocytes.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number6
StatePublished - 1996
Externally publishedYes

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

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