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Prepublished online as a Blood First Edition Paper on June 21, 2002; DOI 10.1182/blood-2002-05-1404.
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Blood, 1 November 2002, Vol. 100, No. 9, pp. 3279-3286
IMMUNOBIOLOGY
Mouse T cells receive costimulatory signals from LIGHT, a TNF
family member
Guixiu Shi,
Hongyu Luo,
Xiaochun Wan,
Theodora W. Salcedo,
Jun Zhang, and
Jiangping Wu
From the Laboratory of Transplantation Immunology and
the Nephrology Service, Centre hospitalier de l'Universite de Montreal
(CHUM), and the Department of Surgery, McGill University, Montreal,
Quebec, Canada; and Human Genome Sciences, Rockville, MD.
LIGHT is a tumor necrosis factor (TNF) family member and is
expressed on activated T cells. Its known receptors are TR2 and LT R
on the cell surface, and TR6/DcR3 in solution. TR6/DcR3 is a secreted
protein belonging to the TNF receptor family. It binds to Fas
ligand (FasL), LIGHT, and TL1A, all of which are TNF family members. In the present study, we report that solid-phase TR6-Fc costimulated proliferation, lymphokine production, and cytotoxicity of
mouse T cells upon T-cell receptor (TCR) ligation. A monoclonal antibody against LIGHT similarly costimulated mouse T cells in their
proliferation response to TCR ligation. These data suggest LIGHT,
although a ligand, can receive costimulation when expressed on the
T-cell surface. Mechanistically, when T cells were activated by TCR and
CD28 co-cross-linking, TCR and rafts rapidly formed caps where they
colocalized. LIGHT rapidly congregated and colocalized with the
aggregated rafts. This provided a molecular base for the signaling
machinery of LIGHT to interact with that of TCR. Indeed, LIGHT
cross-linking enhanced p44/42 mitogen-activated protein kinase
activation after TCR ligation. This study reveals a new function and
signaling event of LIGHT.
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