<i>miR-146a</i> controls the resolution of T cell responses in mice

DOI PDF 被引用文献8件
  • Lili Yang
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1
  • Mark P. Boldin
    Department of Molecular and Cellular Biology, Beckman Research Institute, City of Hope, Duarte, CA 91010 2
  • Yang Yu
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1
  • Claret Siyuan Liu
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1
  • Chee-Kwee Ea
    Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur 50603, Malaysia 3
  • Parameswaran Ramakrishnan
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1
  • Konstantin D. Taganov
    EMD Millipore, Temecula, CA 92590 4
  • Jimmy L. Zhao
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1
  • David Baltimore
    Division of Biology, California Institute of Technology, Pasadena, CA 91125 1

説明

<jats:p>T cell responses in mammals must be tightly regulated to both provide effective immune protection and avoid inflammation-induced pathology. NF-κB activation is a key signaling event induced by T cell receptor (TCR) stimulation. Dysregulation of NF-κB is associated with T cell–mediated inflammatory diseases and malignancies, highlighting the importance of negative feedback control of TCR-induced NF-κB activity. In this study we show that in mice, T cells lacking miR-146a are hyperactive in both acute antigenic responses and chronic inflammatory autoimmune responses. TCR-driven NF-κB activation up-regulates the expression of miR-146a, which in turn down-regulates NF-κB activity, at least partly through repressing the NF-κB signaling transducers TRAF6 and IRAK1. Thus, our results identify miR-146a as an important new member of the negative feedback loop that controls TCR signaling to NF-κB. Our findings also add microRNA to the list of regulators that control the resolution of T cell responses.</jats:p>

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