Differential expression of the B cell-restricted molecule CD22 on neonatalB lymphocytes depending upon antigen stimulation

Citation
D. Viemann et al., Differential expression of the B cell-restricted molecule CD22 on neonatalB lymphocytes depending upon antigen stimulation, EUR J IMMUN, 30(2), 2000, pp. 550-559
Citations number
34
Categorie Soggetti
Immunology
Journal title
EUROPEAN JOURNAL OF IMMUNOLOGY
ISSN journal
00142980 → ACNP
Volume
30
Issue
2
Year of publication
2000
Pages
550 - 559
Database
ISI
SICI code
0014-2980(200002)30:2<550:DEOTBC>2.0.ZU;2-K
Abstract
Newborns respond poorly to certain antigens and produce mainly IgM antibodi es. By flow cytometry we analyzed on neonatal and adult B cells the express ion of CD22, a B cell receptor (BCR)-associated membrane molecule, known as negative modulator of BCR signaling. After T cell-independent (TI-)stimula tion with anti-mu F(ab'), fragments we found a dramatic decrease in the per centage of neonatal CD22(+) B cells and CD22 mean fluorescence intensity (M FI) shift, whereas adult B cells remained unaffected, Survival and prolifer ation rates of neonatal B cells were higher compared to adult B cells where as the degrees of apoptosis and necrosis were comparable. Surprisingly, aft er stimulation with lower doses of anti-CI apoptosis as well as proliferati on increased significantly in contrast to adult B cells. T cell-dependent ( TD)-stimulation with anti-CD40 monoclonal antibody and IL-4 resulted in a d ramatic increase in the percentage of CD22(+) neonatal B cells in contrast to unaffected adult B cells. CD22 MFI shifts showed no significant changes, respectively. The survival rate was higher for adult B cells, whereas apop tosis and cell death were comparable. These results suggest that TI antigen s lower the neonatal BCR signaling threshold via down-regulation of CD22, r esulting in hyperresponsive B cells apt to premature apoptosis. On the othe r hand; up-regulation of CD22 after TD stimulation may allow increased inhi biting influence of CD22 on neonatal ECR signaling, impairing B cell activa tion and differentiation.