Interleukin 15: biology and relevance to human disease

Naturally occurring CD25 1 CD4 1 regulatory T cells are engaged in the maintenance of immunological self-tolerance and down-regulation of various immune responses. Recent studies with mice showed that Foxp3, which encodes the transcription factor Scurfin, is a master regulatory gene for the development and function of CD25 1 CD4 1 regulatory T cells. Here we examined the role of FOXP3 in human CD25 1 CD4 1 regulatory T cells. The FOXP3 gene and its protein product were preferentially expressed in peripheral CD25 1 CD4 1 T cells, in particular CD25 1 CD45RO 1 CD4 1 T cells in normal individuals and, interestingly, in some human T cell leukemia virus type 1-infected T cell lines, which

/pdf/crucial-role-of-foxp3-in-the-development-and-function-of-1lve1fwd8p.pdf

Crucial role of FOXP3 in the development and function of human CD25+CD4+ regulatory T cells

Contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for immunotherapy.

To clarify the status of tax gene, we analyzed human T-cell leukemia virus type-I (HTLV-I) associated cell lines and fresh adult T-cell leukemia (ATL) cells. We compared 2 types of HTLV-I associated cell lines: one was derived from leukemic cells (leukemic cell line) and the other from nonleukemic cells (nonleukemic cell line). Although all nonleukemic cell lines expressed Tax, it could not be detected in 3 of 5 leukemic cell lines, in which nonsense mutation or deletion (60 bp) of tax genes, and DNA methylation in 5'-LTR were identified as the responsible changes. We found such genetic changes of the tax gene in 5 of 47 fresh ATL cases (11%). The tax gene transcripts could be detected in 14 of 41 fresh ATL cases (34%) by RT-PCR. In ATL cases with genetic changes that could not produce Tax protein, the tax gene was frequently transcribed, suggesting that such cells do not need the transcriptional silencing. Although DNA methylation of 5'-LTR was detected in the fresh ATL cases (19 of 28 cases; 68%), the complete methylation associated with transcriptional silencing was observed only in 4 cases. Since partial methylation could not silence the transcription, and the tax gene transcription was not detected in 27 of 41 cases (66%), the epigenetic change(s) other than DNA methylation is considered to play an important role in the silencing.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ijc.20007

Genetic and epigenetic inactivation of tax gene in adult T‐cell leukemia cells

Interleukin 15 (IL-15) mRNA is expressed in a wide variety of tissue types. However, with the exception of some T cell lines, IL-15 transcript expression has not been described in T cells. Herein we demonstrate that IL-15 mRNA can be detected in freshly isolated normal T cells and T cell lines. Furthermore, its expression is 3- to 4-fold higher in human T cell lymphotropic virus type I (HTLV-I)-infected T cells. By using reporter constructs bearing the 5′ regulatory region of the IL-15 gene, we observed a positive correlation between HTLV-I Tax protein expression and IL-15 promoter activity in HTLV-I-infected T cells. Additionally, by using a Jurkat T cell transfectant that expresses Tax under an inducible promoter, we demonstrated that the expression of IL-15 mRNA increased 3-fold as Tax was expressed, suggesting that the Tax protein activates IL-15 transcription. An NF-κB consensus sequence is located at the −75 and −65 region of the IL-15 5′ regulatory region. Mutations in the NF-κB motif or deletion of this sequence abrogated the promoter activity in both HTLV-I-positive and Jurkat Tax-transfectant cells. These data represent evidence for trans-activation of the IL-15 gene by the HTLV-I Tax protein through an NF-κB motif and suggest a potential role for IL-15 in HTLV-I-associated diseases such as adult T cell leukemia and HTLV-I-associated myopathy/tropical spastic paraparesis.

https://www.pnas.org/content/pnas/95/5/2452.full.pdf

Human T cell lymphotropic virus type I Tax protein trans-activates interleukin 15 gene transcription through an NF-κB site

Evidence for the interleukin-2 dependent expansion of leukemic cells in adult T cell leukemia.

adult T cell leukemia Evidence for the interleukin-2 dependent expansion of leukemic cells in

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Evidence for the interleukin-2 dependent expansion of leukemic cells in adult T cell leukemia.

adult T cell leukemia Evidence for the interleukin-2 dependent expansion of leukemic cells in