Splice variants of human FOXP3 are functional inhibitors of human CD4+ T-cell activation
Version of Record online: 10 JUL 2006
Volume 119, Issue 2, pages 203–211, October 2006
How to Cite
Smith, E. L., Finney, H. M., Nesbitt, A. M., Ramsdell, F. and Robinson, M. K. (2006), Splice variants of human FOXP3 are functional inhibitors of human CD4+ T-cell activation. Immunology, 119: 203–211. doi: 10.1111/j.1365-2567.2006.02425.x
- Issue online: 12 JUL 2006
- Version of Record online: 10 JUL 2006
- Received 6 January 2006; revised 26 May 2006; accepted 26 May 2006.
- human T lymphocytes;
- chimeric receptors;
- splice variants;
- inhibition of T-cell activation
FOXP3 has been identified as a key regulator of immune homeostasis. Mutations within the FOXP3 gene result in dysregulated CD4+ T-cell function and elevated cytokine production, leading to lymphoproliferative disease. FOXP3 expression in CD4+ T cells is primarily detected with the CD4+ CD25+ regulatory T-cell population. In humans the protein is detected as a doublet following immunoblot analysis. The lower band of the doublet has been identified as a splice isoform lacking a region corresponding to exon 2. The aim of this study was to investigate whether the splice variant form lacking exon 2 and a new novel splice variant lacking both exons 2 and 7, were functional inhibitors of CD4+ T-cell activation. The data generated showed that full-length FOXP3 and both splice variant forms of the protein were functional repressors of CD4+ T-cell activation.