Published online 12 June 2006 doi:10.1084/jem.20052293
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 7, 1713-1720
Massive and destructive T cell response to homeostatic cue in CD24-deficient lymphopenic hosts
Ou Li1,
Xing Chang1,
Huiming Zhang1,
Ergun Kocak1,
Cheng Ding1,
Pan Zheng1, and
Yang Liu1,2
1 Division of Cancer Immunology, Department of Pathology, The Ohio State University Medical Center, Columbus, OH 43210
2 Center for Infection and Immunity, Institute of Biophysics, Chinese Academy of Science, Beijing 100101, China
CORRESPONDENCE Yang Liu: yang.liu{at}osumc.edu
In response to a lymphopenic cue, T lymphocytes undergo a slow-paced homeostatic proliferation in an attempt to restore T cell cellularity. The molecular interaction that maintains the pace of homeostatic proliferation is unknown. In this study, we report that in lymphopenic CD24-deficient mice, T cells launch a massive proliferation that results in the rapid death of the recipient mice. The dividing T cells have phenotypes similar to those activated by cognate antigens. The rapid homeostatic proliferation is caused by a lack of CD24 on dendritic cells (DCs). Interestingly, although CD24 expression in T cells is required for optimal homeostatic proliferation in the wild-type (WT) host, mice lacking CD24 on all cell types still mount higher homeostatic proliferation than the WT mice. Thus, a lack of CD24 in the nonT host cells bypassed the requirement for T cell expression of CD24 in homeostatic proliferation in the WT host. Our data demonstrate that CD24 expressed on the DCs limits T cell response to homeostatic cue and prevents fatal damage associated with uncontrolled homeostatic proliferation.
Abbreviations used: TREC, TCR rearrangement excision circle; WT, wild type.
O. Li and X. Chang contributed equally to this paper.
X. Chang's, H. Zhang's, C. Ding's, P. Zheng's, and Y. Liu's present address is Division of Immunotherapy, Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109.

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