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International Immunology Advance Access originally published online on July 21, 2008
International Immunology 2008 20(9):1119-1127; doi:10.1093/intimm/dxn070
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

LFA-1 decreases the antigen dose for T cell activation in vivo

Yinan Wang1, Kazuko Shibuya1, Yumi Yamashita1, Jun Shirakawa1, Kai Shibata1, Hirayasu Kai1, Tadashi Yokosuka2, Takashi Saito2, Shin-ichiro Honda1, Satoko Tahara-Hanaoka1 and Akira Shibuya1

1 Department of Immunology, Institute of Basic Medical Sciences and Center for TARA, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Ten-nodai, Tsukuba, Ibaraki 305-8575, Japan
2 Laboratory of Cell Signaling, RIKEN Center for Allergy and Immunology, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan

Correspondence to: K. Shibuya; E-mail: kazukos{at}md.tsukuba.ac.jp

Leukocyte adhesion molecule leukocyte function-associated antigen (LFA)-1 not only mediates intercellular binding but also delivers co-stimulatory signals in T cells. LFA-1 has been shown to decrease the threshold of TCR signal and an antigen dose required for T cell activation and proliferation in vitro. However, physiological significance of the role of LFA-1 in TCR signal has remained unclear. We examined whether LFA-1 decreased the antigen dose for T cell activation in vivo. We showed here that, although collagen-induced arthritis (CIA) could not be induced by immunization and challenge with a standard amount of type-II collagen in LFA-1-deficient mice, a higher dose of the antigen did induce CIA in the absence of LFA-1. We also showed that CD4+ T cells could be primed by immunization with a high, but not low, dose of ovalbumin antigen in LFA-1-deficient mice. These results suggest that LFA-1 decreases the threshold of TCR signal for T cell activation in vivo as well as in vitro. Further studies using TCR-transgenic LFA-1-deficient mice showed that LFA-1 cooperated with TCR in sustained Erk1/2 phosphorylation. Moreover, TCR could induce sustained Erk1/2 phosphorylation in the absence of LFA-1 when T cells were stimulated with a high, but not low, dose of antigen, suggesting that LFA-1 may cooperate with TCR in sustaining Erk1/2 phosphorylation.

Keywords: adhesion molecules, T cell receptors, T cells, Th1/Th2 cells

Transmitting editor: H. Karasuyama

Received 2 October 2007, accepted 3 June 2008.


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