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Journal of Virology, November 2008, p. 11016-11022, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00919-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

CD40 Engagement on Dendritic Cells, but Not on B or T Cells, Is Required for Long-Term Control of Murine Gammaherpesvirus 68{triangledown}

Francesca Giannoni,{dagger} Ashley Shea,{ddagger} Chandra Inglis,§ Lian Ni Lee, and Sally R. Sarawar*

Viral Immunology, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, California 92121

Received 2 May 2008/ Accepted 25 August 2008

CD4 T cells are not essential for primary clearance of replicating murine gammaherpesvirus 68 (MHV-68) but are required for effective long-term control. The virus reactivates in the lungs of major histocompatibility complex class II-deficient (CII–/–) mice that lack functional CD4 T cells. CD40 ligand (CD40L) is upregulated on activated CD4 T cells, and it is thought that CD40-CD40L interactions are an important component of CD4 T-cell help. Our previous studies have shown that agonistic antibodies to CD40 can substitute for CD4 T-cell function in the long-term control of MHV-68. In the present study, we sought to identify the CD40-positive cell type mediating this effect. To address this question, we adoptively transferred MHV-68 peptide-pulsed CII–/– dendritic cells (DC) that had been treated with an agonistic antibody to CD40 into MHV-68-infected CII–/– recipients. Viral reactivation was significantly lower in mice injected with anti-CD40-treated DC than in those injected with control DC or in mice that did not receive any DC. However, in similar experiments with B cells, anti-CD40 treatment had no effect. We also investigated the requirement for CD40 expression on T cells by adoptive transfer of T cells from CD40+/+ or CD40–/– mice into T-cell-deficient recipients that were subsequently infected with MHV-68. The results showed that CD40 expression on T cells is not necessary for preventing viral reactivation. Taken together, our data suggest that CD40 engagement on DC, but not on T or B cells, is essential for effective long-term control of MHV-68.

* Corresponding author. Mailing address: Viral Immunology, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, CA 92121. Phone: (858) 909-5139. Fax: (858) 909-5141. E-mail: ssarawar{at}tpims.org

{triangledown} Published ahead of print on 3 September 2008.

{dagger} Present address: Division of Research Immunology and Bone Marrow Transplantation, CHLA, 4650 Sunset Blvd., Los Angeles, CA 90027.

{ddagger} Present address: Novartis, 500 Technology Square, Cambridge, MA 02139.

§ Present address: Department of Neuroscience, UCSD, 9500 Gilman Drive, #0624, La Jolla, CA 92093-0624.

Journal of Virology, November 2008, p. 11016-11022, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00919-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Krug, L. T., Collins, C. M., Gargano, L. M., Speck, S. H. (2009). NF-{kappa}B p50 Plays Distinct Roles in the Establishment and Control of Murine Gammaherpesvirus 68 Latency. J. Virol. 83: 4732-4748 [Abstract] [Full Text]  
  • Dias, P., Shea, A. L., Inglis, C., Giannoni, F., Lee, L. N., Sarawar, S. R. (2008). Primary Clearance of Murine Gammaherpesvirus 68 by PKC{theta}-/- CD8 T Cells Is Compromised in the Absence of Help from CD4 T Cells. J. Virol. 82: 11970-11975 [Abstract] [Full Text]  


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