The Journal of Experimental Medicine
Keystone Symposia
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Published online 3 July 2006 doi:10.1084/jem.20052495
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 7, 1817-1825
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ARTICLE

 A major histocompatibility complex class I–dependent subset of memory phenotype CD8+ cells

Onur Boyman1,2,3, Jae-Ho Cho1,4, Joyce T. Tan1, Charles D. Surh1, and Jonathan Sprent1,4

1 Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037
2 Division of Immunology and Allergy, University Hospital of Lausanne, CH-1011 Lausanne, Switzerland
3 Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, CH-1066 Epalinges, Switzerland
4 Garvan Institute of Medical Research, Darlinghurst NSW 2010, Australia

CORRESPONDENCE Jonathan Sprent: j.sprent{at}garvan.org.au

Most memory phenotype (MP) CD44hi CD8+ cells are resting interleukin (IL)-15–dependent cells characterized by high expression of the IL-2/IL-15 receptor ß (CD122). However, some MP CD8+ cells have a CD122lo phenotype and are IL-15 independent. Here, evidence is presented that the CD122lo subset of MP CD8+ cells is controlled largely by major histocompatibility complex (MHC) class I molecules. Many of these cells display surface markers typical of recently activated T cells (CD62Llo, CD69hi, CD43hi, and CD127lo) and show a high rate of background proliferation. Cells with this phenotype are highly enriched in common {gamma} chain–deficient mice and absent from MHC-I–/– mice. Unlike CD122hi CD8+ cells, CD122lo MP CD8+ cells survive poorly after transfer to MHC-I–/– hosts and cease to proliferate. Although distinctly different from typical antigen-specific memory cells, CD122lo MP CD8+ cells closely resemble the antigen-dependent memory CD8+ cells found in chronic viral infections.

Abbreviations used: MP, memory phenotype; tg, transgenic.

J.T. Tan's present address is Anadys Pharmaceuticals, Inc., San Diego, CA 92121.


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