LTβR signaling in dendritic cells induces a type I IFN response that is required for optimal clonal expansion of CD8+ T cells

Proc Natl Acad Sci U S A. 2011 Feb 1;108(5):2046-51. doi: 10.1073/pnas.1014188108. Epub 2011 Jan 18.

Abstract

During an immune response, antigen-bearing dendritic cells (DCs) migrate to the local draining lymph node and present antigen to CD4(+) helper T cells. Antigen-activated CD4(+) T cells then up-regulate TNF superfamily members including CD40 ligand and lymphotoxin (LT)αβ. Although it is well-accepted that CD40 stimulation on DCs is required for DC licensing and cross-priming of CD8(+) T-cell responses, it is likely that other signals are integrated into a comprehensive DC activation program. Here we show that a cognate interaction between LTαβ on CD4(+) helper T cells and LTβ receptor on DCs results in unique signals that are necessary for optimal CD8(+) T-cell expansion via a type I IFN-dependent mechanism. In contrast, CD40 signaling appears to be more critical for CD8(+) T-cell IFNγ production. Therefore, different TNF family members provide integrative signals that shape the licensing potential of antigen-presenting DCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD8-Positive T-Lymphocytes / cytology*
  • Cell Division*
  • Cell Line
  • Humans
  • Interferon Type I / biosynthesis*
  • Lymphocyte Activation
  • Lymphotoxin beta Receptor / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Signal Transduction*

Substances

  • Interferon Type I
  • Lymphotoxin beta Receptor