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International Immunology, Vol. 15, No. 7, pp. 861-870, July 2003
© 2003 Japanese Society for Immunology

LIGHT-deficiency impairs CD8+ T cell expansion, but not effector function

Jinqi Liu1, Clint S. Schmidt2, Feisha Zhao1, Angela J. Okragly1, Andrew Glasebrook2, Niles Fox1, Elizabeth Galbreath1, Qing Zhang1, Ho Yeong Song1, Songqing Na2 and Derek D. Yang1

1 Department of Bio-Research and Technologies and Proteins, and 2 Department of Inflammation and Immunomodulation Research, Eli Lilly & Co., Indianapolis, IN 46285, USA

The first two authors contributed equally to this work
Correspondence to: S. Na; E-mail: na_songqing{at}lilly.com or D. D. Yang; E-mail: yang_derek_di{at}lilly.com
Transmitting editor: R. Medzhitov

LIGHT, a newly identified member of the tumor necrosis factor (TNF) family, is expressed on activated T lymphocytes. To evaluate how LIGHT contributes to T cell functions, we generated LIGHT-deficient (LIGHT–/–) mice using gene targeting. Disruption of LIGHT significantly reduced CD8+ T cell-cycle progression, leading to reduced proliferation to anti-CD3, anti-CD3/anti-CD28 or allogeneic stimulation, whereas proliferation of CD4+ T cells remained unchanged. In contrast to the observed proliferative defects, isolated CD8+ T cells from LIGHT–/– mice displayed normal cytotoxic effector function development when compared to wild-type CD8+ T cells. Underlying a potential mechanism of reduced CD8+ T cell proliferation, LIGHT–/– CD8+ T cells displayed reduced surface levels of CD25 and a diminished ability to proliferate in response to exogenous IL-2. Furthermore, addition of IL-12 to LIGHT–/– CD8+ T cell cultures could not ameliorate this proliferative defect. These results reveal a potential mechanism of action for LIGHT as a positive regulator of CD8+ T cell expansion, but not lytic effector function development.

Keywords: CD8+, effector function, LIGHT, T cell expansion


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