PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10669119-6 1999 Cyclosporine A was also the most effective drug downregulating the expression of accessory molecules (CD54, CD58, CD80 and CD86). Cyclosporine 0-14 CD58 molecule Homo sapiens 108-112 7570986-5 1995 This nonresponsiveness induced by anti-LFA-3 or anti-IL-2/IL-2R could be overcome by the incorporation of cyclosporine during the first-round stimulation or by incorporation of IL-2 during the second-round stimulation. Cyclosporine 106-118 CD58 molecule Homo sapiens 39-44 7833280-2 1995 The treatment with cyclosporine was based on the hypothesis that immune-mediated bone-marrow damage is the common pathogenetic mechanism of aplasia and PNH, with lack of GPI-linked ligands for an immune attack (i.e. LFA-3, CD58) rendering PNH cells a growth advantage over other bone marrow cells. Cyclosporine 19-31 CD58 molecule Homo sapiens 216-221 7833280-2 1995 The treatment with cyclosporine was based on the hypothesis that immune-mediated bone-marrow damage is the common pathogenetic mechanism of aplasia and PNH, with lack of GPI-linked ligands for an immune attack (i.e. LFA-3, CD58) rendering PNH cells a growth advantage over other bone marrow cells. Cyclosporine 19-31 CD58 molecule Homo sapiens 223-227 1679377-7 1991 Finally, costimulation by PI-LFA-3, but not by EC, is completely suppressed by cyclosporine A. Cyclosporine 79-93 CD58 molecule Homo sapiens 29-34