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RelB suppresses type I Interferon signaling in dendritic cells

Irene Saha1, Hemant Jaiswal1, Richa Mishra2

  • 1Laboratory of Innate Immunity, National Institute of Immunology, New Delhi, India.

Cellular Immunology
|February 12, 2020
PubMed

Insights

Relb acts as a novel negative regulator of type I interferon signaling in dendritic cells. This finding reveals a new mechanism for controlling immune responses and dendritic cell development.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Type I Interferon (IFN) signaling is crucial for dendritic cell (DC) development and function.
  • Hyperactive type I IFN signaling can impede the development of the cDC2 subtype.
  • Relb is a known transcription factor essential for cDC2 development.

Purpose of the Study:

  • To investigate the role of Relb in modulating type I IFN signaling within dendritic cells.
  • To understand the molecular mechanisms by which Relb influences IFN responses.
  • To determine the impact of Relb on cDC2 development in the context of IFN signaling.

Main Methods:

  • Analysis of type I IFN signaling in Relb-expressing and Relb-deficient dendritic cells (FL-DCs, cDC2 cultures).
  • Assessment of Interferon-Stimulated Genes (ISGs) and IκBα levels.
  • Utilizing Ifnar1 knockout mice to study cDC2 development in the absence of IFN signaling.

Main Results:

  • Relb suppresses homeostatic type I IFN signaling in cDC2 cultures.
  • TLR stimulation induced RelB, which correlated with decreased IFN signatures and ISG levels.
  • Relb's inhibitory effect on IFN signaling is mediated by increased IκBα levels.
  • Relb deficiency led to dampened antiviral responses due to elevated ISG levels.
  • cDC2 developmental defects in Relb null mice were rescued in an Ifnar1-deficient background.

Conclusions:

  • Relb functions as a novel negative regulator of the type I IFN signaling pathway.
  • Relb fine-tunes type I IFN signaling, impacting dendritic cell development, particularly the cDC2 subtype.
  • This study elucidates a new mechanism controlling immune homeostasis and DC subtype differentiation.

Keywords:
Dendritic cell differentiationInterferon stimulated genes (ISGs)NF-κB signalingRelBType I Interferon (IFN)

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