Regulatory Functioning T Cell Population Contributing to the Mediation of Endotoxin Tolerance

    • Suzuki Nobuaki
    • Division of Clinical Infection Control and Prevention, Graduate School of Medical and Dental Sciences, Niigata University
    • Tanabe Yoshinari
    • Division of Clinical Infection Control and Prevention, Graduate School of Medical and Dental Sciences, Niigata University

    • Oota Kyuma
    • Division of Clinical Infection Control and Prevention, Graduate School of Medical and Dental Sciences, Niigata University
    • Gejyo Fumitake
    • Division of Clinical Infection Control and Prevention, Graduate School of Medical and Dental Sciences, Niigata University

Abstract

Endotoxin tolerance (ET) has been considered to develop mainly due to the hyporesponsiveness of monocytes and macrophages. Weexamined the role ofT cells in ET mice. T cells derived from ET mice showed a decreased level of interferon-γ (IFN-γ) production in comparison to those from the control mice when T cells were cocultured with peritoneal exudate cells (PEC) adherent cells from the controls or lipopolysaccharide (LPS)- injected ET mice. After anti-CD3 stimulation, IFN-γ induction by T cells derived from ET mice was significantly decreased in comparison to those from the control mice. On the other hand, interleukin-10 (IL-10) secretion by T cells derived from ET mice was higher than in those of the control mice. When T cells with a high CD62L expression (CD62Lhigh T cells) were co-cultured with PEC adherent cells, the secretion of IFN-γ tended to decrease more than when these were co-cultured with T cells with a low CD62L expression (CD62Llow T cells). Our data suggest that T cells expressing CD62Lhigh T cells in ET mice can play a suppressive role in antigen-presenting cells through their cytokine production.

Journal

Acta medica et biologica   [List of Volumes]

Acta medica et biologica 55(2), 45-53, 2007-06  [Table of Contents]

Niigata University

Codes

  • NII Article ID (NAID) :
    110006447108
  • NII NACSIS-CAT ID (NCID) :
    AA00508361
  • Text Lang :
    ENG
  • ISSN :
    05677734
  • Databases :
    NII-ELS