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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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NF-kB-dependent Signaling Pathway02:26

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Optimized Protocol for Efficient Transfection of Dendritic Cells without Cell Maturation
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Published on: July 8, 2011

Type I IFN regulate DC turnover in vivo.

Fabrizio Mattei1, Laura Bracci, David F Tough

  • 1Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy. fabrizio.mattei@iss.it

European Journal of Immunology
|June 23, 2009
PubMed
Summary

Type I interferons (IFN-I) regulate dendritic cell (DC) turnover by influencing their apoptosis, proliferation, and migration. Loss of the IFN-I receptor in mice reduces DC turnover, impacting immune cell function.

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Dendritic cells (DCs) are crucial antigen-presenting cells activating T cells during infection.
  • Type I interferons (IFN-I) are produced by DCs and can act in an autocrine fashion to activate them.

Purpose of the Study:

  • To investigate the role of IFN-I in regulating the turnover and lifespan of DCs.
  • To understand how IFN-I signaling affects DC proliferation, apoptosis, and migration.

Main Methods:

  • Utilized type I IFN receptor knockout (IFNAR KO) and wild-type (WT) mice.
  • Employed BrdU labeling kinetics to assess DC turnover in vivo.
  • Conducted in vitro cultures of bone marrow (BM) precursor cells and splenic DCs.
  • Analyzed DC generation, apoptosis, and migratory ability.

Main Results:

  • IFNAR KO mice exhibited reduced DC turnover, particularly the CD8alpha(+) subset, compared to WT mice.
  • In vitro, IFNAR KO BM precursors generated DCs less efficiently and with reduced migratory capacity.
  • IFN-I exposure in vivo and in vitro increased splenic DC turnover and apoptosis, especially in CD8alpha(+) DCs.

Conclusions:

  • IFN-I are significant regulators of DC turnover in vivo.
  • IFN-I modulate DC apoptosis, proliferation, and migration, influencing overall DC lifespan and immune response.