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Chronic lymphocytic leukemia cells induce defective LFA1–directed T-cell motility by altering Rho GTPase signaling that is reversible with lenalidomide by Alan G. Ramsay, Rachel Evans, Shahryar Kiaii, Lena Svensson, Nancy Hogg, and John G. Gribben Blood Volume 121(14):2704-2714 April 4, 2013 ©2013 by American Society of Hematology T cells from CLL patients exhibit impaired LFA-1 – mediated motility that can be induced in healthy T cells via direct tumor cell contact. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology The immunomodulatory drug lenalidomide repairs the LFA-1 – mediated motility defect in CLL patient T cells. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology Lenalidomide increases extended intermediate- and high-affinity LFA-1 expression on CLLderived T cells and rescues their firm adhesion to CD54. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology Lenalidomide targets Rho GTPase signaling in T cells from CLL patients. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology CLL tumor cells induce altered LFA-1 – mediated Rho GTPase activity. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology Schematic representation of CLL-induced Rho GTPase signaling defects in T cells that suppress LFA-1 activation signaling and migration and how this is reversible with lenalidomide. Alan G. Ramsay et al. Blood 2013;121:2704-2714 ©2013 by American Society of Hematology
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