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CARDIOVASCULAR
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Volume 3, 1998, No 2 |
Abstract:
Background: Monitoring for the responses to alloantigens
presented either by the direct or the indirect presentation
pathway have been reported to be of clinical value after kidney
transplantation. Amongst others the level of these responses may
be dependent on the immunosuppressive treatment. Methods: We
studied these pathways in peripheral blood mononuclear cells
(PBMC) of cardiac transplant patients in an attempt to find a
correlation between these tests and the clinical status of the
patients. Results: Both before and after transplantation,
comparable proportions of PBMC samples reacted in MLC (mixed
lymphocyte cultures) to nondepleted donor spleen cells (direct
route), but never to donor cells depleted for antigen-presenting
cells (indirect route). In contrast, the latter route could
easily be activated by a nominal antigen (tetanus toxoid (TET))
and persisted after transplantation. After transplantation the
proportion of PBMC samples responding to TET was significantly
suppressed, irrespective of the occurrence of rejection.
Nevertheless, analyzing the level of PBMC reactivity, both the
immune responses via the direct and indirect presentation route
increased when cyclosporine A (CsA) levels inadvertently
decreased to inadequate concentrations and acute rejection was
diagnosed. During immunological quiescence high and low
responders could be detected to both the direct and indirect
pathway, while graft vascular disease (GVD) was only positively
correlated with a higher PBMC reactivity to indirect presented
TET antigens. Conclusion: The level of PBMC reactivity via both
the direct and indirect presentation pathway is correlated with
acute rejection early after transplantation, while only the
indirect pathway was associated with GVD. These tests might be
used as a tool for selecting patients in which tapering of
immunosuppresion can safely be performed.
Keywords:
heart transplantation, antigen presentation pathways,
immunosuppression, acute rejection, graft vascular disease
Address for Correspondence:
Reference:
(CVE. 1998; 3 (2): 105-111)
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