Stimulation of XXXX bone marrow stromal cell @entity669 kinases and @entity650 production by contact with B lymphocytes.

@entity1 @entity650 @entity2109 @entity1759 @entity2393 @entity3818 @entity4725 @entity5690 @entity669 @entity16445
The interaction of normal @entity1 B cell precursors with the bone marrow (BM) stromal cells that support their growth and maturation is mediated by adhesion of B cell @entity5690 / @entity2393 (alpha 4 beta 1 integrin or VLA-4) to stromal cell signal transduction, we generated @entity5690 -deficient variants of the RAMOS early b @entity2109 cell line. RAMOS was chosen due to its lack of expression of @entity16445 (alpha 5 integrin) and @entity1759 , which could potentially interact with stromal cells or their extracellular matrix. In contrast to the parental RAMOS cell line, @entity5690 -deficient RAMOS cell lines did not adhere to primary @entity1 BM stromal cells. @entity669 phosphorylation of several stromal cell proteins was stimulated within 5 to 10 min of contact with either @entity5690 -expressing or @entity5690 -deficient RAMOS. These proteins included a 110-kDa substrate tentatively identified as @entity3818 . In contrast, mAb cross-linking of stromal cell @entity4725 had no significant effect on protein @entity669 phosphorylation. @entity650 production by stromal cells was enhanced up to fourfold over 3 days when stromal cells were cultured in contact with RAMOS cells, regardless of @entity5690 expression. Stromal cell @entity650 production was not significantly enhanced by RAMOS cells cultured above the stromal cells in Transwell inserts. Thus, we have demonstrated through the use of paired @entity5690 -expressing and @entity5690 -deficient RAMOS cell lines that protein @entity669 kinase activity and @entity650 production by primary @entity1 BM stromal cells can be enhanced in a manner that is dependent on B cell contact but independent of @entity5690 -mediated adhesion. These results indicate the potential for B cells to interact with cells in their microenvironment and activate feedback mechanisms mediated by stromal cells, which may regulate lymphopoiesis.
