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

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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 246))

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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© 1999 Springer-Verlag Berlin Heidelberg

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Taher, T.E.I. et al. (1999). Cross-talk Between CD44 and c-Met in B cells. In: Melchers, F., Potter, M. (eds) Mechanisms of B Cell Neoplasia 1998. Current Topics in Microbiology and Immunology, vol 246. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60162-0_4

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  • DOI: https://doi.org/10.1007/978-3-642-60162-0_4

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64283-8

  • Online ISBN: 978-3-642-60162-0

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