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The Journal of Immunology, 2002, 168: 4832-4835.
Copyright © 2002 by The American Association of Immunologists


Cutting Edge

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

Koji Tamada*, Jian Ni{ddagger}, Gefeng Zhu*, Michele Fiscella{ddagger}, Baiqin Teng{ddagger}, Jan M. A. van Deursen{dagger} and Lieping Chen2,*

Departments of * Immunology and {dagger} Pediatrics and Adolescent Medicine, Mayo Clinic, Rochester, MN 55905; and {ddagger} Human Genome Sciences, Rockville, MD 20850

Interactions of LIGHT and its receptors, herpesvirus entry mediator on T cells and lymphotoxin {beta} 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 V{beta}8+ T cells in naive LIGHT+/+ and LIGHT-/- mice was identical, V{beta}8+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 V{beta}8+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.




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