International Immunology, Vol. 15, No. 7, pp. 817-826,
July 2003
© 2003 Japanese Society for Immunology
CD154–CD40-independent up-regulation of B7-2 on splenic antigen-presenting cells and efficient T cell priming by staphylococcal enterotoxin A
1 Section of Immunobiology and 2 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA 3 Department of Immunology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan 4 Abramson Family Cancer Research Institute, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Correspondence to: R. A. Flavell; E-mail: richard.flavell{at}yale.edu
Transmitting editor: H. Karasuyama
It has been demonstrated that in vivo T cell priming requires CD154–CD40 interaction, which is suggested to be critical in the induction of co-stimulatory activities on antigen-presenting cells (APC). In the current study, we demonstrate that in vivo administration of a high dose of a superantigen, staphylococcal enterotoxin A (SEA), could up-regulate B7-2 on most splenic APC independently of the CD154–CD40 interaction, followed by efficient expansion of SEA-reactive Vß3+ T cells in CD154- or CD40-deficient mice. However, the CD154–CD40 interaction may be involved in SEA-mediated T cell activation, since a contribution of the CD154–CD40 interaction was observed when a lower dose of SEA was injected. CD154-independent T cell priming by SEA appeared also independent of the TRANCE–RANK pathway, which was shown to be capable of mediating CD154-independent activation of naive T cells during the infection of some viruses. These results indicate that SEA, which provokes rapid and efficient T cell responses without adjuvant, could utilize multiple CD154/TRANCE-independent pathways, to prime T cells.
Keywords: cellular activation, co-stimulation, superantigen, T lymphocyte