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15 January 2005

Volume 191, Number 2
The Journal of Infectious Diseases 2005;191:243–254
© 2004 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19102-0014$15.00
DOI: 10.1086/426944
MAJOR ARTICLE

Expression of Cutaneous Lymphocyte–Associated Antigen and E‐selectin Ligand by Circulating Human Memory CD4+ T Lymphocytes Specific for Herpes Simplex Virus Type 2

Julio C. González,1

William W. Kwok,6

Anna Wald,1,3

Christopher L. McClurkan,4

Jay Huang,4 and

David M. Koelle1,2,4,5,6

Departments of 1Medicine, 2Pathobiology, 3Epidemiology, and 4Laboratory Medicine, University of Washington, 5Fred Hutchinson Cancer Research Center, and 6Benaroya Research Institute, Seattle, Washington

Virus‐specific memory T lymphocytes traffic to sites of viral infection. Herpes simplex virus (HSV) type 2–specific CD4+ and CD8+ T lymphocytes differ with regard to their homing kinetics to infected tissues. We studied the expression of cutaneous lymphocyte–associated antigen (CLA) and E‐selectin ligand (ESL) by HSV‐2–specific CD4+ T lymphocytes. Virus‐reactive T lymphocytes were identified ex vivo by CD154 or interferon‐γ up‐regulation. We detected selective expression of CLA by HSV‐2–reactive CD4+ T lymphocytes, but at levels lower than those we previously observed for CD8+ T lymphocytes. Short‐term HSV‐2–reactive CD4+ lines generated from peripheral‐blood mononuclear cells preferentially express CLA, compared with cytomegalovirus‐ or influenza‐specific cells. CLA is expressed by HSV‐2–reactive cells that are initially CLA negative before restimulation. Short‐term culture‐expanded HSV‐2–specific CD4+ T lymphocytes also selectively express ESL. These findings have implications for the optimization of vaccines for HSV and other cutaneous pathogens.

Received 10 May 2004; accepted 9 August 2004; electronically published 15 December 2004.

Reprints or correspondence: Dr. David M. Koelle, Harborview Medical Center, Box 359690, 325 Ninth Ave., Seattle, WA 98104 ().

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  • Presented in part: 42nd Interscience Conference on Antimicrobial Agents and Chemotherapy, San Diego, 27–30 September 2002 (abstract V‐916).

    Financial support: National Institutes of Health (grants AI50132 and AI30731); the present work was conducted while J.C.G. was a Pfizer Postdoctoral Fellow.

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