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PubMed1995

CAM--a novel immunosuppressive agent.

This is an initial study of the immunosuppressive efficacy of CAM, a derivative of mycophenolic acid, in a rat heart allograft model when the major histocompatibility complex was fully incompatible, and its effect in improving heart allograft survival compared with mycophenolate mofetil (MMF, RS-61443). CAM or MMF was administered orally from day 1 following the allografting for 40 days. The median survival times (MST) were 6 days in rats with no immunosuppressive drug (control group; n = 6), 83 days with CAM 10 mg/kg (n = 6), and > 100 days with both 20 mg/kg (n = 7), and 30 mg/kg (n = 10). With MMF, in contrast, MST was 9, 17, 35, days with 10, 20, 30 mg/kg/day, respectively. All grafts in the CAM 30 mg/kg-treated group survived for more than 100 days after grafting, and, furthermore, CAM was also more effective than MMF in prolongation of the heart graft survival in rats at each dose. Rats with long-surviving cardiac allografts (30 mg/kg; CAM) accepted skin grafts from the donor-strain but rejected them from the third-party strain, suggesting that donor-specific tolerance was induced by CAM. In the tolerant rats, proliferative response against donor-type alloantigen was not impaired as compared with naive WKAH rats. In contrast, CML assay showed that T cells obtained from the rats bearing permanently accepted F344 heart grafts had less cytotoxic activity to the donor-type target, and the frequency of CTL precursor against donor-type alloantigen was also reduced.

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PubMed2003

Current immunosuppressive agents: efficacy, side effects, and utilization.

Advances in immunosuppressive therapy over the past decade have led to dramatic improvements in graft survival. With the development of new agents, the focus of the transplant community is to establish regimens that maintain excellent graft survival rates but with fewer toxicities including infection, nephrotoxicity, malignancy, and cosmetic effects. Examples include the use of steroid-free protocols and calcineurin avoidance regimens, which are currently being studied by NAPRTCS. The ultimate goal of transplant immunosuppressive therapy is the induction of tolerance. As we learn more about immune function from basic and clinical research, tolerance to allografts seems a more reachable goal.

Abatacept↗
PubMedDate not supplied

Cellular signaling mechanisms for stimulation of growth hormone secretion and growth hormone primary transcripts by immunosuppressant agents, FK506 and cyclosporin A, in cultured rat pituitary cells.

Although an immunosuppressant, FK506, has been known to stimulate growth hormone (GH) release from rat somatotropes, the cellular signaling mechanism is unknown. In the present study, intracellular signaling pathways were investigated for FK506- and cyclosporin A (CsA)-induced GH release in cultured rat anterior pituitary cells. Northern and Western blot analysis revealed that the FK506-binding protein (FKBP12) and the CsA-binding protein (cyclophilin A) exist at the mRNA and protein level in the rat anterior pituitary tissue. FK506 and CsA increased GH release in a dose-dependent manner and inhibited calcineurin (CaN) activity in the cultured pituitary cells. The third immunosuppressant, rapamycin (RP), inhibited the FK506-induced GH release, although RP alone had no effect. Protein kinase A (PKA) inhibitors, H-89 and HA-1004 and EGTA blocked FK506- and CsA-induced GH release. TGF-beta did not alter basal GH release, but inhibited FK506-induced GH release. GH primary transcripts were increased by FK506, and the effects were blocked by H-89 and HA-1004. These results suggest that the immunosuppressants, FK506 and CsA, stimulate GH release by inhibiting CaN activity which results in the activation of the PKA system in the rat somatotropes. TGF-beta receptors might be involved in FK506-induced GH release as a separate pathway. FK506 also stimulates GH primary transcripts via a PKA-dependent mechanism in a manner similar to its effects on GH release.

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