Runx3 inhibits IL-4 production in T cells via physical interaction with NFAT

Sung Ho Lee, Hyung Min Jeong, Jin Myung Choi, Young Chang Cho, Tae Sung Kim, Kwang Youl Lee, Bok Yun Kang

    Research output: Contribution to journalArticlepeer-review

    18 Citations (Scopus)

    Abstract

    Interleukin (IL)-4 plays a key role in T helper 2 (Th2) cell differentiation favoring humoral immune response. Regulation of IL-4 gene expression, therefore, is critically important for Th2 dependent responses and Th2 dominant disorders. In T cells, IL-4 gene expression is regulated positively or negatively by a combination of several transcription factors. Recently, enhanced IL-4 production was reported in Runx3 knockout mice; this implies negative regulation of IL-4 by Runx3. Runx proteins are transcription factors that have a Runt domain and have essential functions in development. In this study, the molecular mechanism that downregulates IL-4 expression was investigated. Runx3 inhibited IL-4 production in EL-4 T cells stimulated with PMA/ionomycin. Runx3-mediated IL-4 inhibition was NFAT-dependent, and Runx3 was physically associated with NFAT. Therefore, our results suggest that the interaction between NFAT and Runx3 is a mechanism that causes the negative regulation of IL-4, along with previously reported repression by T-bet.

    Original languageEnglish
    Pages (from-to)214-217
    Number of pages4
    JournalBiochemical and biophysical research communications
    Volume381
    Issue number2
    DOIs
    Publication statusPublished - 2009 Apr 3

    Bibliographical note

    Funding Information:
    This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2008-531-E00105) and Grant No. RTI05-01-01 from the Regional Technology Innovation Program of the Ministry of Commerce, Industry and Energy (MOCIE), Republic of Korea.

    Keywords

    • IL-4
    • NFAT
    • Runx3

    ASJC Scopus subject areas

    • Biophysics
    • Biochemistry
    • Molecular Biology
    • Cell Biology

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