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This process depends on metabolic energy, active signaling and protein tyrosine kinase activity. The adhesion pathway influenced by this signaling event is neuraminidase sensitive. The anti\u2010adhesive signaling program is activated in B cell lines with a mature phenotype, <jats:italic>e.g.<\/jats:italic> normal B cells from spleen and tonsil. In contrast, cell lines with a pre\u2010B cell phenotype and normal B cells from peripheral blood are refractory to MHC class II\u2010mediated regulation of adhesion. These results extend to neoplastic cells from patients with lymphopro\u2010liferative diseases representing different stages of B cell maturation. These results suggest that MHC class II\u2010mediated signals regulate B cell adhesion in a developmentally programmed fashion; this might have implications for clinical behavior of B cell malignancies.<\/jats:p>","DOI":"10.1002\/eji.1830271031","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T04:08:42Z","timestamp":1172808522000},"page":"2688-2695","source":"Crossref","is-referenced-by-count":9,"title":["Anti\u2010adhesive signals are mediated via major histocompatibility complex class II molecules in normal and neoplastic human B cells: Correlation with B cell differentiation stage"],"prefix":"10.1002","volume":"27","author":[{"given":"Els J. 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