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The role of 2 FOXP3 isoforms in the generation of human CD4(+) Tregs
The role of 2 FOXP3 isoforms in the generation of human CD4(+) Tregs JOURNAL OF CLINICAL INVESTIGATION Allan, S. E., Passerini, L., Bacchetta, R., Crellin, N., Dai, M. Y., ORBAN, P. C., Ziegler, S. F., Roncarolo, M. G., Levings, M. K. 2005; 115 (11): 3276-3284Abstract
Little is known about the molecules that control the development and function of CD4+ CD25+ Tregs. Recently, it was shown that the transcription factor FOXP3 is necessary and sufficient for the generation of CD4+ CD25+ Tregs in mice. We investigated the capacity of FOXP3 to drive the generation of suppressive CD4+ CD25+ Tregs in humans. Surprisingly, although ectopic expression of FOXP3 in human CD4+ T cells resulted in induction of hyporesponsiveness and suppression of IL-2 production, it did not lead to acquisition of significant suppressor activity in vitro. Similarly, ectopic expression of FOXP3delta2, an isoform found in human CD4+ CD25+ Tregs that lacks exon 2, also failed to induce the development of suppressor T cells. Moreover, when FOXP3 and FOXP3delta2 were simultaneously overexpressed, although the expression of several Treg-associated cell surface markers was significantly increased, only a modest suppressive activity was induced. These data indicate that in humans, overexpression of FOXP3 alone or together with FOXP3delta2 is not an effective method to generate potent suppressor T cells in vitro and suggest that factors in addition to FOXP3 are required during the process of activation and/or differentiation for the development of bona fide Tregs.
View details for DOI 10.1172/JCI24685
View details for Web of Science ID 000233022100037
View details for PubMedID 16211090