• Sandra Lopez-Vergès, Jeffrey M Milush, Brian S Schwartz, Marcelo J Pando, Jessica Jarjoura, Vanessa A York, Jeffrey P Houchins, Steve Miller, Sang-Mo Kang, Phillip J Norris, Douglas F Nixon, and Lewis L Lanier.
• Department of Microbiology and Immunology and Cancer Research Institute, University of California, San Francisco, CA 94143, USA.
• Proc. Natl. Acad. Sci. U.S.A. 2011 Sep 6; 108 (36): 14725-32.

AbstractDuring human CMV infection, there is a preferential expansion of natural killer (NK) cells expressing the activating CD94-NKG2C receptor complex, implicating this receptor in the recognition of CMV-infected cells. We hypothesized that NK cells expanded in response to pathogens will be marked by expression of CD57, a carbohydrate antigen expressed on highly mature cells within the CD56(dim)CD16(+) NK cell compartment. Here we demonstrate the preferential expansion of a unique subset of NK cells coexpressing the activating CD94-NKG2C receptor and CD57 in CMV(+) donors. These CD57(+)NKG2C(hi) NK cells degranulated in response to stimulation through their NKG2C receptor. Furthermore, CD57(+)NKG2C(hi) NK cells preferentially lack expression of the inhibitory NKG2A receptor and the inhibitory KIR3DL1 receptor in individuals expressing its HLA-Bw4 ligand. Moreover, in solid-organ transplant recipients with active CMV infection, the percentage of CD57(+)NKG2C(hi) NK cells in the total NK cell population preferentially increased. During acute CMV infection, the NKG2C(+) NK cells proliferated, became NKG2C(hi), and finally acquired CD57. Thus, we propose that CD57 might provide a marker of "memory" NK cells that have been expanded in response to infection.

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