Abstract:
BACKGROUND:Dendritic cells (DC) can exert powerful immune stimulatory as well as regulatory functions and are therefore important tools for therapeutic strategies. Dexamethasone (Dex) was previously shown to inhibit DC maturation and to induce regulatory properties both in vitro and in vivo. Here, we investigated the immunoregulatory role of DexDC in two different rat acute rejection models of kidney transplantation. METHODS:Rat DC were generated from BN and DA bone marrow in the presence of the corticosteroid, Dex. The function of Dex-modulated DC was analyzed in vitro and in vivo, using a BN to LEW and a DA to LEW renal transplantation model in the absence of other forms of immunosuppression. T cells of transplanted rats were isolated and restimulated with donor mature DC (lipopolysaccharide [LPS] or CD40L activated). T-cell responsiveness was analyzed by proliferative capacity and IFN-gamma production. RESULTS:Stimulation of Dex-modulated rat DC with LPS resulted in normal IL-10 production, whereas synthesis of IL-12 was impaired. In accordance, the capacity of LPS-DexDC to stimulate T-cell activation was decreased. In both renal transplantation models, treatment with donor-derived LPS-DexDC induced a significant donor-specific T-cell hyporesponse. However, pretreatment did not result in a prolonged graft survival. CONCLUSIONS:In two fully mismatched kidney transplantation models, donor-derived LPS-DexDC induce a donor-specific T-cell hyporesponse. However, in this setting allograft survival was not improved, suggesting an important role for T cells with indirect alloreactivity. Understanding the underlying mechanism involved in the rejection process will improve the development of a cell-based immunotherapy.
journal_name
Transplantationjournal_title
Transplantationauthors
Stax AM,Gelderman KA,Schlagwein N,Essers MC,Kamerling SW,Woltman AM,van Kooten Cdoi
10.1097/TP.0b013e31818a6682subject
Has Abstractpub_date
2008-11-15 00:00:00pages
1275-82issue
9eissn
0041-1337issn
1534-6080pii
00007890-200811150-00018journal_volume
86pub_type
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