PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10933163-3 2000 In the present study, we investigated in vitro whether CsA could alter the antigenicity of activated porcine aortic endothelial cells (PAECs) by reducing class I and class II MHC antigen expression. Cyclosporine 55-58 major histocompatibility complex, class I, C Homo sapiens 175-178 10933163-4 2000 METHODS: The effect of CsA on MHC antigen expression during tumor necrosis factor (TNF)-alpha- or lymphocyte-mediated PAEC activation was evaluated in vitro by flow cytometry and correlated to the ability of porcine ECs to promote human T lymphocyte proliferation. Cyclosporine 23-26 major histocompatibility complex, class I, C Homo sapiens 30-33 10933163-5 2000 The effect of CsA on class II MHC antigen mRNA expression was also analyzed and related to class II transcriptional activator (CIITA) mRNA expression. Cyclosporine 14-17 major histocompatibility complex, class I, C Homo sapiens 30-33 10933163-6 2000 RESULTS: Flow cytometry analysis showed that TNF-alpha-mediated induction of class II MHC antigen expression on PAECs was completely inhibited by CsA, whereas expression of class I MHC was reduced by 50%. Cyclosporine 146-149 major histocompatibility complex, class I, C Homo sapiens 86-89 10933163-10 2000 Pretreatment of PAECs with CsA for 4 hr before coculture with human peripheral blood leukocytes efficiently blocked the induction on PAECs of E-selectin and class II MHC antigens and inhibited overexpression of class I antigens. Cyclosporine 27-30 major histocompatibility complex, class I, C Homo sapiens 166-169 10933163-13 2000 CONCLUSION: Our study indicates that CsA could play a role in preventing porcine MHC antigens being directly presented to human T lymphocytes by xenogeneic ECs. Cyclosporine 37-40 major histocompatibility complex, class I, C Homo sapiens 81-84 2651768-10 1989 The most likely candidates are the immunosuppressive drugs, such as cyclosporine and prednisone, which decrease MHC antigen expression. Cyclosporine 68-80 major histocompatibility complex, class I, C Homo sapiens 112-115 9156650-5 1997 The lysosomotropic amines, at low concentrations, in combination with the T cell-specific agent, cyclosporin A, synergistically suppresses the T cell response to MiHC and MHC in mouse and in human. Cyclosporine 97-110 major histocompatibility complex, class I, C Homo sapiens 171-174 7643135-5 1995 Immunosuppression with Cyclosporin A prevented invasion of T-lymphocytes and allowed differentiation of implanted myoblasts into myofibres as well as down-regulation of MHC expression. Cyclosporine 23-36 major histocompatibility complex, class I, C Homo sapiens 169-172 7643135-13 1995 It is suggested that the start of immune reaction following Cyclosporin A withdrawal is initiated by remaining small amounts of donor MHC molecules, possibly related to the continuous proliferation of the cell-lined-derived donor myoblasts. Cyclosporine 60-73 major histocompatibility complex, class I, C Homo sapiens 134-137 1371950-1 1992 Cyclosporin A (CsA) was tested for its modulatory effects on the mIgM-mediated signaling of G0*-associated increases in class II MHC expression, G1-related RNA synthesis, and S phase-related DNA synthesis in human B cells. Cyclosporine 15-18 major histocompatibility complex, class I, C Homo sapiens 129-132 2667211-9 1989 Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine. Cyclosporine 0-12 major histocompatibility complex, class I, C Homo sapiens 93-96 2667211-9 1989 Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine. Cyclosporine 0-12 major histocompatibility complex, class I, C Homo sapiens 167-170 2667211-9 1989 Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine. Cyclosporine 235-247 major histocompatibility complex, class I, C Homo sapiens 167-170 3061073-3 1988 CsA treatment prevented the induction of MHC antigen within allografts. Cyclosporine 0-3 major histocompatibility complex, class I, C Homo sapiens 41-44 2647926-3 1989 Our hypothesis was that changes in histocompatibility (MHC) expression induced by immunosuppressive therapy with cyclosporine plays an important role in directing an immune response to the arterial bed. Cyclosporine 113-125 major histocompatibility complex, class I, C Homo sapiens 55-58 3061073-4 1988 Whereas at day 4, both rejecting and CsA treated grafts showed donor class I MHC expression on duct epithelium and islet cells, only rejecting grafts displayed class I MHC induction on acinar cells. Cyclosporine 37-40 major histocompatibility complex, class I, C Homo sapiens 77-80 3061073-5 1988 Rejecting grafts showed strong induction of class II MHC antigen expression on duct epithelium from day 4 onward but this was completely prevented by CsA treatment. Cyclosporine 150-153 major histocompatibility complex, class I, C Homo sapiens 53-56 3061073-8 1988 These results show a favorable effect of CsA on rat fetal pancreas allografts with a reduction in MHC antigen expression within the graft and prolonged survival of insulin-rich endocrine tissue. Cyclosporine 41-44 major histocompatibility complex, class I, C Homo sapiens 98-101 2425369-0 1986 Inhibition of MHC product induction may contribute to the immunosuppressive action of ciclosporin. Cyclosporine 86-97 major histocompatibility complex, class I, C Homo sapiens 14-17