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Transmission of survival signals through Delta-like 1 on activated CD4+ T cells

Takahiro Furukawa1,2, Chieko Ishifune1, Shin-Ichi Tsukumo1

  • 1Department of Immunology &Parasitology, Graduate School of Medicine, Tokushima University, Tokushima, Japan.

Scientific Reports
|September 24, 2016
PubMed

Insights

The Notch ligand Dll1 is crucial for CD4+ T cell survival, independent of cis-inhibition. This finding reveals a new mechanism regulating adaptive immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Notch signaling regulates CD4+ T cell effector functions and survival.
  • The role of Notch ligands on T cells is not fully understood, particularly regarding cis-inhibition.
  • Notch ligands on T cells may have distinct signaling roles.

Purpose of the Study:

  • To investigate the function of the Notch ligand Dll1 on CD4+ T cells.
  • To determine if Dll1 signaling is required for T cell survival.
  • To elucidate the role of Dll1 in adaptive immune responses and autoimmune diseases.

Main Methods:

  • Co-transfer of CD4+ T cells from Dll1 knockout (Dll1-/-) and control mice into recipient mice.
  • Induction of experimental autoimmune encephalitis (EAE) in recipient mice.
  • Analysis of T cell survival, Notch target gene expression, and clinical scores.

Main Results:

  • CD4+ T cells from Dll1-/- mice showed a rapid decline in survival compared to controls.
  • Dll1 deficiency in T cells did not affect Notch target gene expression, suggesting intact cis- Notch signaling.
  • Overexpression of Dll1 intracellular domain partially rescued survival in Dll1-deficient T cells.
  • Dll1-/- mice exhibited reduced EAE severity.

Conclusions:

  • Dll1 is an independent regulator of Notch signaling essential for activated CD4+ T cell survival.
  • Dll1 plays a significant role in adaptive immunity and T cell homeostasis.
  • These findings offer new insights into the physiological functions of Notch ligands and immune regulation.

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