Potential mechanisms of action of interferon-alpha in CML.

摘要: Treatment with interferon-alpha (IFN-alpha) adequately controls the leukemic cell mass in majority of newly diagnosed patients chronic myeloid leukemia (CML). However, degree response ranges from no 'hematologic' to complete suppression clone. The mechanism(s) by which IFN-alpha elicits these responses is unknown, but vitro studies have indicated that might function (1) selective toxicity against clone, (2) enhancement 'immune' regulation, and (3) modulation bone marrow microenvironmental regulation hematopoiesis. Using clonogenic assays we were unable demonstrate selectively inhibited proliferation CML progenitor cells. We also found difference expression LFA-3 on normal or CD34+ panning co-culturing hematopoietic cells monolayers stromal cells, grown without IFN-alpha, enhanced adhesion progenitors whereas was essentially unaffected. This associated a reduction neuraminic acid levels extracellular matrix overlying Therefore, it possible one mechanisms exerts its regulatory effect clone through cell-microenvironmental interactions.