International Immunology, Vol. 15, No. 1, pp. 127-136,
January 2003
© 2003 Japanese Society for Immunology
CD4 T cell priming in dendritic cell-deficient mice
1 Department of Medicine and Cancer Center, University of California San Diego, 9500 Gilman Drive, La Jolla CA 92093-0837, USA 2 Digital Gene Technologies, La Jolla, CA 92037, USA 3 Division of Immunochemistry, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92121, USA 4 Laboratoire d’Immunite Cellulaire Anti-Virale, Institut Pasteur, 75724 Paris, France
Correspondence to: M. Zanetti; E-mail:mzanetti{at}ucsd.edu
Transmitting editor: S. M. Hedrick
Bone marrow (BM) chimeras (BMC) generated from mice carrying a null (–/–) mutation in the relB gene of the NF-
B family represent an ideal model for in vivo studies on the role of dendritic cells (DC) in the adaptive immune response. The spleen and lymph nodes (LN) of relB–/– BMC contain a small number of residual DC, mainly CD8
+, that fail to up-regulate MHC class II and co-stimulatory molecules after stimulation in vitro. Moreover, residual spleen DC of relB–/– BMC have a 4-fold decrease in the ability to uptake and process soluble model antigen, ovalbumin (OVA), and failed to prime CD4 and CD8 T cells in vitro and in vivo. In addition, they also failed to present OVA peptide to OT-II transgenic T lymphocytes at a normal 1:10 (stimulator:responder) cell ratio. In spite of these multiple DC defects, relB–/– BMC immunized with plasmid DNA targeted to the spleen as the site of immune induction develop a specific CD4+ T cell response comparable to that of relB competent mice. These data demonstrate that CD4 + T cells can be primed in the absence of functional DC and suggest that relB may gauge the T cell response in vivo.
Keywords: dendritic cell, in vivo transgenesis, relB, T cell immunity
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