Cutting Edge: Selective Impairment of CD8+ T Cell Function in Mice Lacking the TNF Superfamily Member LIGHT

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.