Cross-talk between CD44 and c-Met in B cells

TEI Taher, R Van Der Voort, L Smit… - Mechanisms of B Cell …, 1999 - Springer
TEI Taher, R Van Der Voort, L Smit, RMJ Keehnen, EJM Schilder-Tol, M Spaargaren…
Mechanisms of B Cell Neoplasia 1998: Proceedings of the Workshop held at the …, 1999Springer
Activation of naive B cells in the T cell areas of the secondary lymphoid tissues initiates T
cell dependent humoral immune responses. As a consequence of this primary B cell
activation, germinal center (GC) cell precursors migrate into B cell follicles where they
engage T cells and follicular dendritic cells (FDC), and differentiate into plasma cells or
memory B cells. Both the homing of B cells to the GC and their interaction with FDC critically
depend on integrin-mediated adhesion. We have recently identified the growth and motility …
Abstract
Activation of naive B cells in the T cell areas of the secondary lymphoid tissues initiates T cell dependent humoral immune responses. As a consequence of this primary B cell activation, germinal center (GC) cell precursors migrate into B cell follicles where they engage T cells and follicular dendritic cells (FDC), and differentiate into plasma cells or memory B cells. Both the homing of B cells to the GC and their interaction with FDC critically depend on integrin-mediated adhesion. We have recently identified the growth and motility factor, hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the c-met-encoded receptor tyrosine kinase, as a novel paracrine signaling pathway regulating B cell adhesion within the GC microenvironment [22]. The c-Met protein is expressed on B cells localized in the dark zone of the GC (centroblasts) and is induced by combined CD40 and B-cell receptor ligation. Stimulation of c-Met with HGF/SF, which is produced at high levels by tonsillar stromal cells and FDC, leads to enhanced integrin-mediated adhesion of B cells to fibronectin and VCAM-1 [22].
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