The Journal of Experimental Medicine
Keystone Symposia
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Published online December 26, 2006
doi:10.1084/jem.20061303
The Journal of Experimental Medicine, Vol. 204, No. 1, 25-31
The Rockefeller University Press, 0022-1007 $30.00
© 2006 Pua et al.
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BRIEF DEFINITIVE REPORT

 A critical role for the autophagy gene Atg5 in T cell survival and proliferation

Heather H. Pua1, Ivan Dzhagalov1, Mariana Chuck1, Noboru Mizushima2,3, and You-Wen He1

1 Department of Immunology, Duke University Medical Center, Durham, NC 27710
2 Department of Bioregulation and Metabolism, Tokyo Metropolitan Institute of Medical Sciences, Tokyo 113-8613, Japan
3 SORST, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan

CORRESPONDENCE You-Wen He: he000004{at}mc.duke.edu

Macroautophagy (hereafter referred to as autophagy) is a well-conserved intracellular degradation process. Recent studies examining cells lacking the autophagy genes Atg5 and Atg7 have demonstrated that autophagy plays essential roles in cell survival during starvation, in innate cell clearance of microbial pathogens, and in neural cell maintenance. However, the role of autophagy in T lymphocyte development and survival is not known. Here, we demonstrate that autophagosomes form in primary mouse T lymphocytes. By generating Atg5–/– chimeric mice, we found that Atg5-deficient T lymphocytes underwent full maturation. However, the numbers of total thymocytes and peripheral T and B lymphocytes were reduced in Atg5 chimeras. In the periphery, Atg5–/– CD8+ T lymphocytes displayed dramatically increased cell death. Furthermore, Atg5–/– CD4+ and CD8+ T cells failed to undergo efficient proliferation after TCR stimulation. These results demonstrate a critical role for Atg5 in multiple aspects of lymphocyte development and function and suggest that autophagy may be essential for both T lymphocyte survival and proliferation.


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