The Journal of Experimental Medicine
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Published online 29 August 2005 doi:10.1084/jem.20050821
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 5, 637-650
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ARTICLE

 Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection

Ganesh A. Kolumam1,2, Sunil Thomas1,2, Lucas J. Thompson1,2, Jonathan Sprent3, and Kaja Murali-Krishna1,2

1 Department of Immunology, University of Washington, Seattle, WA 98195
2 Washington National Primate Center, University of Washington, Seattle, WA 98195
3 Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037

CORRESPONDENCE Kaja Murali-Krishna: mkaja{at}u.washington.edu

T cell expansion and memory formation are generally more effective when elicited by live organisms than by inactivated vaccines. Elucidation of the underlying mechanisms is important for vaccination and therapeutic strategies. We show that the massive expansion of antigen-specific CD8 T cells that occurs in response to viral infection is critically dependent on the direct action of type I interferons (IFN-Is) on CD8 T cells. By examining the response to infection with lymphocytic choriomeningitis virus using IFN-I receptor–deficient (IFN-IR0) and –sufficient CD8 T cells adoptively transferred into normal IFN-IR wild-type hosts, we show that the lack of direct CD8 T cell contact with IFN-I causes >99% reduction in their capacity to expand and generate memory cells. The diminished expansion of IFN-IR0 CD8 T cells was not caused by a defect in proliferation but by poor survival during the antigen-driven proliferation phase. Thus, IFN-IR signaling in CD8 T cells is critical for the generation of effector and memory cells in response to viral infection.

Abbreviations used: BrdU, bromodeoxy-uridine; IFN-I, type I IFN; LCMV, lymphocytic choriomeningitis virus.


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