JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baribaud, F.
Right arrow Articles by Acha-Orbea, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baribaud, F.
Right arrow Articles by Acha-Orbea, H.

 Previous Article  |  Next Article 

Journal of Virology, October 1999, p. 8403-8410, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Role of Dendritic Cells in the Immune Response Induced by Mouse Mammary Tumor Virus Superantigen

Frédéric Baribaud,1,* Ivan Maillard,1 Sonia Vacheron,2,3 Thomas Brocker,4 Heidi Diggelmann,1 and Hans Acha-Orbea2,3

Institute of Microbiology, University of Lausanne, CH-1011 Lausanne,1 Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges,2 and Ludwig Institute for Cancer Research, Lausanne Branch,3 CH-1066 Epalinges, Switzerland, and Universität Freiburg, Medizinische Universitätsklinik, Abteilung Innere Medizin I, Medizinische Molekularbiologie, D-79106 Freiburg, Germany4

Received 4 March 1999/Accepted 9 July 1999

After mouse mammary tumor virus (MMTV) infection, B lymphocytes present a superantigen (Sag) and receive help from the unlimited number of CD4+ T cells expressing Sag-specific T-cell receptor Vbeta elements. The infected B cells divide and differentiate, similarly to what occurs in classical B-cell responses. The amplification of Sag-reactive T cells can be considered a primary immune response. Since B cells are usually not efficient in the activation of naive T cells, we addressed the question of whether professional antigen-presenting cells such as dendritic cells (DCs) are responsible for T-cell priming. We show here, using MMTV(SIM), a viral isolate which requires major histocompatibility complex class II I-E expression to induce a strong Sag response in vivo, that transgenic mice expressing I-E exclusively on DCs (I-Ealpha DC tg) reveal a strong Sag response. This Sag response was dependent on the presence of B cells, as indicated by the absence of stimulation in I-Ealpha DC tg mice lacking B cells (I-Ealpha DC tg µMT-/-), even if these B cells lack I-E expression. Furthermore, the involvement of either residual transgene expression by B cells or transfer of I-E from DCs to B cells was excluded by the use of mixed bone marrow chimeras. Our results indicate that after priming by DCs in the context of I-E, the MMTV(SIM) Sag can be recognized on the surface of B cells in the context of I-A. The most likely physiological relevance of the lowering of the antigen threshold required for T-cell/B-cell collaboration after DC priming is to allow B cells with a low affinity for antigen to receive T-cell help in a primary immune response.

* Corresponding author. Present address: Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, 806 Abramson, 34th and Civic Center Blvd., Philadelphia, PA 19104. Phone: (215) 573-7532. Fax: (215) 573-2883. E-mail: fbaribau{at}mail.med.upenn.edu.

Journal of Virology, October 1999, p. 8403-8410, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 1999 by the American Society for Microbiology. All rights reserved.