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Journal of Virology, March 2006, p. 2863-2872, Vol. 80, No. 6
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.6.2863-2872.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Innate Immune Responses to Herpes Simplex Virus Type 2 Influence Skin Homing Molecule Expression by Memory CD4+ Lymphocytes

David M. Koelle,1,2,3,4,5* Jay Huang,2 Michael T. Hensel,3 and Christopher L. McClurkan2

Department of Medicine, University of Washington, Seattle, Washington,1 Department of Laboratory Medicine, University of Washington, Seattle, Washington,2 Department of Pathobiology, University of Washington, Seattle, Washington,3 Fred Hutchinson Cancer Research Center, Seattle, Washington,4 Benaroya Research Institute, Seattle, Washington5

Received 23 August 2005/ Accepted 19 December 2005

Herpes simplex virus (HSV) infections of humans are characterized by intermittent, lytic replication in epithelia. Circulating HSV-specific CD4 T cells express lower levels of preformed cutaneous lymphocyte-associated antigen (CLA), a skin-homing receptor, than do circulating HSV-specific CD8 T cells but, paradoxically, move into infected skin earlier than CD8 cells. Memory CD4 T cells develop strong and selective expression of CLA and E-selectin ligand while responding to HSV antigen in vitro. We now show that interleukin-12, type I interferon, and transforming growth factor beta are each involved in CLA expression by memory HSV type 2 (HSV-2)-specific CD4 T cells in peripheral blood mononuclear cells (PBMC). A reduction of the number of monocytes and dendritic cells from PBMC reduces CLA expression by HSV-2-responsive CD4 lymphoblasts, while their reintroduction restores this phenotype, identifying these cells as possible sources of CLA-promoting cytokines. Plasmacytoid dendritic cells are particularly potent inducers of CLA on HSV-reactive CD4 T cells. These observations are consistent with cooperation between innate and acquired immunity to promote a pattern of homing receptor expression that is physiologically appropriate for trafficking to infected tissues.

* Corresponding author. Mailing address: Harborview Medical Center, Mail Stop 359690, 325 Ninth Ave., Seattle, WA 98104. Phone: (206) 341-5207. Fax: (206) 341-5203. E-mail: viralimm{at}u.washington.edu.

Journal of Virology, March 2006, p. 2863-2872, Vol. 80, No. 6
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.6.2863-2872.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Donaghy, H., Bosnjak, L., Harman, A. N., Marsden, V., Tyring, S. K., Meng, T.-C., Cunningham, A. L. (2009). Role for Plasmacytoid Dendritic Cells in the Immune Control of Recurrent Human Herpes Simplex Virus Infection. J. Virol. 83: 1952-1961 [Abstract] [Full Text]  
  • Jing, L., Chong, T. M., Byrd, B., McClurkan, C. L., Huang, J., Story, B. T., Dunkley, K. M., Aldaz-Carroll, L., Eisenberg, R. J., Cohen, G. H., Kwok, W. W., Sette, A., Koelle, D. M. (2007). Dominance and Diversity in the Primary Human CD4 T Cell Response to Replication-Competent Vaccinia Virus. J. Immunol. 178: 6374-6386 [Abstract] [Full Text]  
  • Diaz, G. A., Koelle, D. M. (2006). Human CD4+ CD25high Cells Suppress Proliferative Memory Lymphocyte Responses to Herpes Simplex Virus Type 2.. J. Virol. 80: 8271-8273 [Abstract] [Full Text]  


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