Age-associated decline in effective immune synapse formation of CD4(+) T cells is reversed by vitamin E supplementation

J Immunol. 2007 Feb 1;178(3):1443-9. doi: 10.4049/jimmunol.178.3.1443.

Abstract

Aging is associated with reduced IL-2 production and T cell proliferation. Vitamin E supplementation, in aged animals and humans, increases cell division and IL-2 production by naive T cells. The immune synapse forms at the site of contact between a T cell and an APC and participates in T cell activation. We evaluated whether vitamin E affects the redistribution of signaling proteins to the immune synapse. Purified CD4(+) T cells, from the spleens of young and old mice, were treated with vitamin E before stimulation with a surrogate APC expressing anti-CD3. Using confocal fluorescent microscopy, we observed that CD4(+) T cells from old mice were significantly less likely to recruit signaling proteins to the immune synapse than cells from young mice. Vitamin E increased the percentage of old CD4(+) T cells capable of forming an effective immune synapse. Similar results were found following in vivo supplementation with vitamin E. When compared with memory cells, naive T cells from aged mice were more defective in immune synapse formation and were more responsive to vitamin E supplementation. These data show, for the first time, that vitamin E significantly improves age-related early T cell signaling events in naive CD4(+) T cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Aging / immunology*
  • Animals
  • Antigen Presentation / drug effects*
  • Antigen-Presenting Cells
  • CD4-Positive T-Lymphocytes / cytology
  • CD4-Positive T-Lymphocytes / drug effects*
  • CD4-Positive T-Lymphocytes / immunology*
  • Cell Communication / drug effects
  • Cell Communication / immunology
  • Coculture Techniques
  • Dietary Supplements
  • Mice
  • Mice, Inbred C57BL
  • Signal Transduction / drug effects
  • Signal Transduction / immunology
  • Vitamin E / pharmacology*
  • Vitamin E / therapeutic use

Substances

  • Vitamin E