Short-term anti-CD25 monoclonal antibody administration down-regulated CD25 expression without eliminating the neogenetic functional regulatory T cells in kidney transplantation

CD4⁺CD25⁺ forkhead box P3 (FoxP3)⁺regulatory T (Treg) cells are generated and play a key role in the induction and maintenance of transplant tolerance in organ recipients. It has been proposed that interleukin (IL)-2/IL-2 receptor (IL-2R) signalling was essential for the development and proliferatio...

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Veröffentlicht in:Clinical and experimental immunology 2009-03, Vol.155 (3), p.496-503
Hauptverfasser: Wang, Z, Shi, B.-Y, Qian, Y.-Y, Cai, M, Wang, Q
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Sprache:eng
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Zusammenfassung:CD4⁺CD25⁺ forkhead box P3 (FoxP3)⁺regulatory T (Treg) cells are generated and play a key role in the induction and maintenance of transplant tolerance in organ recipients. It has been proposed that interleukin (IL)-2/IL-2 receptor (IL-2R) signalling was essential for the development and proliferation of antigen-activated T cells that included both effector T cells and Treg cells. Basiliximab (Simulect[trade mark sign]), a chimeric monoclonal antibody directed against the α-chain of the IL-2R (CD25), can be expected to not only affect alloreactive effector T cells, but also reduce the number and function of Treg cells. We therefore examined the effect of basiliximab induction therapy on the number and function of the Treg cells in renal recipients. Basiliximab decreased the percentage of CD4⁺CD25⁺T cells, but failed to influence the percentage of CD4⁺FoxP3⁺ Treg cells. The cellular CD25 expression was decreased significantly by basiliximab injection, but CD4⁺CD25⁺ T cells was not depleted from the circulating pool through monoclonal antibody activation-associated apoptosis. Functional analysis revealed that inhibitory function of Treg cells from recipients with basiliximab injection was not significantly different from recipients without injection. These data indicate that the functional Treg population may not be influenced by short-term basiliximab treatment.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.2008.03847.x