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

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.