Cutting edge: Selective impairment of CD8+ T cell function in mice lacking the TNF superfamily member LIGHT

Koji Tamada, Jian Ni, Gefeng Zhu, Michele Fiscella, Baiqin Teng, Jan M.A. Van Deursen, Lieping Chen

Research output: Contribution to journalArticle

84 Scopus citations

Abstract

Interactions of LIGHT and its receptors, herpesvirus entry mediator on T cells and lymphotoxin β receptor on stromal cells, are implicated in the regulation of lymphoid organogenesis, costimulation of T cells, and activation of dendritic cells. In this work we report that LIGHT-deficient mice had normal lymphoid organs with T cells and APCs that normally responded to Ag stimulation and normally stimulated T cells. Although the number of Vβ8+ T cells in naive LIGHT+/+ and LIGHT-/- mice was identical, Vβ8+CD8+ T cell proliferation in response to staphylococcal enterotoxin B was significantly lower in LIGHT-/- mice. Consistently, induction and cytokine secretion of CD8+ CTL to MHC class I-restricted peptide was also reduced in LIGHT-/- mice. However, the proliferative response of Vβ8+ CD4+ T cells to staphylococcal enterotoxin B was comparable in LIGHT-/- and LIGHT+/+ mice. Our results suggest that LIGHT is required for activation of normal CD8+ T cells but not CD4+ T cells.

Original languageEnglish (US)
Pages (from-to)4832-4835
Number of pages4
JournalJournal of Immunology
Volume168
Issue number10
DOIs
StatePublished - May 15 2002

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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