Direct cellular interaction with activated @entity404 (+) T cells overcomes XXXX of @entity1072 in vitro.

@entity1 @entity6306 @entity404 @entity42428 @entity1199 @entity2936 @entity11603 @entity1072 @entity5893 @entity32998 @entity1453 @entity7937 @entity2731 @entity2071 @entity3646
The proliferative response of clonal B cells from @entity1 with @entity1072 ( @entity1072 ) is drastically reduced compared to normal B lymphocytes stimulated via the B cell antigen receptor complex or by @entity2936 ligation. In the present study we demonstrate that @entity6306 of CLL-B cells can be overcome by stimulatory pathways mediated by activated @entity404 (+) T cells. In contrast to @entity2936 ligation, costimulation with activated T cells promotes a proliferative response in CLL-B cells identical to that in normal B cells. Furthermore, coculture with activated T cells improved survival of CLL-B cells in vitro. Differentiation of CLL-B cells into IgM producing cells was promoted, as well. However, the capacity for IgM secretion remained impaired compared to that of normal B cells. For T-cell-mediated B cell activation direct cellular contact with activated T helper cells is absolutely required. Prevention of @entity2936 / @entity11603 interaction by @entity2936 antibody caused only partial inhibition of B cell activation, suggesting that additional signals are involved in T-B cell interaction. Whereas interruption of the ligand pairs @entity1453 / @entity2071 , @entity5893 / @entity42428 , @entity2731 / @entity32998 had no influence, the addition of @entity7937 antibody completely inhibited B cell activation by activated T cells. In costimulation with cellular signals the presence of B-cell-tropic cytokines, such as @entity1199 and @entity3646 , was required to optimize @entity1072 proliferation, as demonstrated by the use of neutralizing antibodies. We conclude from these results that proliferative @entity6306 by CLL-B cells can be circumvented by antigen-nonspecific signals in addition to @entity2936 which are mediated by direct contact with activated T helper cells.
