• ja Interferon regulatory factor-4 activates IL-2 and IL-4 promoters in cooperation with c-Rel.
    • Shindo, Hisakazu
    • Yasui, Kiyoshi
    • Yamamoto, Kazuo
    • Honma, Kiri
    • Yui, Katsuyuki
    • Kohno, Tomoko
    • Ma, Yuhua
    • Chua, Koon Jiew
    • Kubo, Yoshinao
    • Aihara, Hitoshi
    • Ito, Takashi
    • Nagayasu, Takeshi
    • Matsuyama, Toshifumi
    • Hayashi, Hideki
  • Copyright © 2011 Elsevier Ltd. All rights reserved.
  • Other Adult T-cell leukemia/lymphoma (ATLL)
  • Other C-Rel
  • Other IL-2
  • Other IL-4
  • Other Interferon regulatory factor (IRF)-4
  • Other Interferon regulatory factor (IRF)-4 is a member of the IRF transcription factor family, whose expression is primarily restricted to lymphoid and myeloid cells. In T-cells, IRF-4 expression is induced by T-cell receptor (TCR) cross-linking or treatment with phorbol-12-myristate-13-acetate (PMA)/Ionomycin, and IRF-4 is thought to be a critical factor for various functions of T-cells. To elucidate the IRF-4 functions in human adult T-cell leukemia virus type 1 (HTLV-1)-infected T-cells, which constitutively express IRF-4, we isolated IRF-4-binding proteins from T-cells, using a tandem affinity purification (TAP)-mass spectrometry strategy. Fourteen proteins were identified in the IRF-4-binding complex, including endogenous IRF-4 and the nuclear factor-kappaB (NF-κB) family member, c-Rel. The specific association of IRF-4 with c-Rel was confirmed by immunoprecipitation experiments, and IRF-4 was shown to enhance the c-Rel-dependent binding and activation of the interleukin-4 (IL-4) promoter region. We also demonstrated that IL-2 production was also enhanced by exogenously-expressed IRF-4 and c-Rel in the presence of P/I, in T-cells, and that the optimal IL-2 and IL-4 productions in vivo was IRF-4-dependent using IRF-4-/- mice. These data provide molecular evidence to support the clinical observation that elevated expression of c-Rel and IRF-4 is associated with the prognosis in adult T-cell leukemia/lymphoma (ATLL) patients, and present possible targets for future gene therapy.
  • Other identifier:Cytokine, 56(3), pp.564-572; 2011
Publisher Elsevier Ltd.
    Created2020-12-22 , Issued2011-12
  • eng
Resource Type journal article
Version Type AM
Identifier URI
  • isIdenticalTo PMID 21890374
  • isIdenticalTo DOI
    • ISSN 1043-4666
    • ISSN 1096-0023
      • Cytokine 56(3), 564-572
Oaidate 2021-02-17