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Infection and Immunity, August 2006, p. 4505-4511, Vol. 74, No. 8
0019-9567/06/$08.00+0     doi:10.1128/IAI.00088-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Gamma Interferon Secretion by Human V{gamma}2V{delta}2 T Cells after Stimulation with Antibody against the T-Cell Receptor plus the Toll-Like Receptor 2 Agonist Pam3Cys

Carl O. Deetz,1,2 Andrew M. Hebbeler,1,3 Nadia A. Propp,1 Cristiana Cairo,1 Illia Tikhonov,1,{dagger} and C. David Pauza1*

Institute of Human Virology, University of Maryland Biotechnology Institute, Baltimore, Maryland,1 Graduate Program in Molecular Medicine, University of Maryland, Baltimore, Maryland,2 Department of Molecular Microbiology and Immunology, University of Maryland, Baltimore, Maryland3

Received 17 January 2006/ Returned for modification 3 March 2006/ Accepted 4 May 2006

Circulating V{gamma}2V{delta}2 T-cell populations in healthy human beings are poised for rapid responses to bacterial or viral pathogens. We asked whether V{gamma}2V{delta}2 T cells use the Toll-like receptor (TLR) family to recognize pathogen-associated molecular pattern molecules and to regulate cell functions. Analysis of expanded V{gamma}2V{delta}2 T-cell lines showed the abundant presence of TLR2 mRNA, implying that these receptors are important for cell differentiation or function. However, multiple efforts to detect TLR2 protein on the cell surface or in cytoplasmic compartments gave inconsistent results. Functional assays confirmed that human V{gamma}2V{delta}2 T cells could respond to the TLR2 agonist (S)-(2,3-bis(palmitoyloxy)-(2RS)-propyl)-N-palmitoyl-(R)-Cys-(S)-Ser(S)-Lys4-OH trihydrochloride (Pam3Cys), but the response required coincident stimulation through the {gamma}{delta} T-cell receptor (TCR). Dually stimulated cells produced higher levels of cytoplasmic or cell-free gamma interferon and showed increased expression of the lysosome-associated membrane protein CD107a on the cell surface. A functional TLR2 that requires coincident TCR stimulation may increase the initial potency of V{gamma}2V{delta}2 T-cell responses at the site of infection and promote the rapid development of subsequent acquired antipathogen immunity.

* Corresponding author. Mailing address: Institute of Human Virology, University of Maryland Biotechnology Institute, 725 West Lombard Street, Baltimore, MD 21201. Phone: (410) 706-1367. Fax: (410) 706-6212. E-mail: pauza{at}umbi.umd.edu.

Editor: J. F. Urban, Jr.

{dagger} Present address: Sanofi Pasteur, Swiftwater, Pa.

Infection and Immunity, August 2006, p. 4505-4511, Vol. 74, No. 8
0019-9567/06/$08.00+0     doi:10.1128/IAI.00088-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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