Specific tissue invasion, localisation and matrix modification in hairy-cell leukemia.

HCs have a distinctive profile of matrix-binding integrin receptors which partly reflects their activated nature. HCs show differing functional responses to individual adhesive proteins, and these are mediated by particular integrin heterodimers. In particular, HCs are motile on Vitronectin (VN), and this motility is mediated by alpha v beta 3. HCs are immobile but actively spread on Fibronectin (FN) and this response is mediated by beta 1 integrins. M-CSF enhances the mobility (chemotaxis and chemokinesis) of HCs, and this response is partly mediated by alpha v beta 3. HCs synthesise and assemble fibronectin and this is, at least partly, the cause of the distinctive bone marrow fibrosis of hairy-cell leukaemia.