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Suppression of NF-κB and downstream XBP1 by DcR3 contributes to a decrease in antibody secretion.

Po-Chun Liu1, Szu-Ying Huang1, Kuo-I Lin2

  • 1Institute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Taipei City, Taiwan.

Journal of Immunology (Baltimore, Md. : 1950)
|March 12, 2025
PubMed
Summary
This summary is machine-generated.

Decoy receptor 3 (DcR3) impairs antibody production by reducing X-box binding protein 1 (XBP1) expression in B cells. This mechanism involves inhibiting NF-κB activation, ultimately decreasing antibody secretion.

Keywords:
NF-κBX-box binding protein 1antibody secretiondecoy receptor 3humoral response

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Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • Decoy receptor 3 (DcR3) is a soluble receptor modulating immune cell functions.
  • DcR3 is known to suppress B cell proliferation and ameliorate autoimmune diseases.
  • The precise role of DcR3 in regulating antibody production remains unclear.

Purpose of the Study:

  • To investigate the mechanism by which DcR3 regulates antibody production.
  • To determine if DcR3 affects T cell-dependent antibody responses.
  • To elucidate the molecular pathways involved in DcR3-mediated regulation of antibody secretion.

Main Methods:

  • Utilized a DcR3 transgenic mouse model for in vivo studies.
  • Performed in vitro assays using DcR3-Fc fusion protein with B cells.
  • Assessed T cell-dependent antibody responses, B cell proliferation, and antibody secretion.
  • Analyzed the expression of secretory Igh, Xbp1, and NF-κB activity.
  • Investigated the role of X-box binding protein 1 (XBP1) in DcR3-mediated effects.

Main Results:

  • DcR3 transgenic mice exhibited impaired T cell-dependent antibody responses.
  • DcR3-Fc fusion protein attenuated T cell-dependent antibody production in vitro.
  • DcR3-Fc reduced the expression of secretory Igh and Xbp1 in activated B cells.
  • DcR3-Fc inhibited NF-κB activity and XBP1 promoter activity, crucial for Xbp1 expression.
  • Restoring spliced XBP1 partially rescued the antibody production defect.

Conclusions:

  • DcR3 impairs antibody production by suppressing NF-κB activation and subsequent XBP1 expression in B cells.
  • This reduction in XBP1 leads to decreased antibody secretion, both in vitro and in vivo.
  • DcR3's role extends beyond proliferation suppression to directly impacting antibody production mechanisms.