The Journal of Experimental Medicine
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Published online April 16, 2007
doi:10.1084/jem.20070176
The Journal of Experimental Medicine, Vol. 204, No. 5, 1095-1106
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Soares et al.
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ARTICLE

 A subset of dendritic cells induces CD4+ T cells to produce IFN-{gamma} by an IL-12–independent but CD70-dependent mechanism in vivo

Helena Soares1, HaeNa Waechter1, Nicholas Glaichenhaus3, Evelyne Mougneau3, Hideo Yagita4, Olga Mizenina1, Diana Dudziak2, Michel C. Nussenzweig2, and Ralph M. Steinman1

1 Laboratory of Cellular Physiology and Immunology and Chris Browne Center, and 2 Laboratory of Molecular Immunology and the Howard Hughes Institute, The Rockefeller University, New York, NY 10021
3 E03-44, Institut National de la Sainté et de la Recherche Médicale, University of Nice-Sophia Antipolis, 06560 Valbonne, France
4 Department of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan

CORRESPONDENCE Ralph M. Steinman: steinma{at}mail.rockefeller.edu

Interferon (IFN)-{gamma}, a cytokine critical for resistance to infection and tumors, is produced by CD4+ helper T lymphocytes after stimulation by cultured dendritic cells (DCs) that secrete a cofactor, interleukin (IL)-12. We have identified a major IL-12–independent pathway whereby DCs induce IFN-{gamma}–secreting T helper (Th)1 CD4+ T cells in vivo. This pathway requires the membrane-associated tumor necrosis family member CD70 and was identified by targeting the LACK antigen from Leishmania major within an antibody to CD205 (DEC-205), an uptake receptor on a subset of DCs. Another major DC subset, targeted with 33D1 anti-DCIR2 antibody, also induced IFN-{gamma} in vivo but required IL-12, not CD70. Isolated CD205+ DCs expressed cell surface CD70 when presenting antigen to T cell receptor transgenic T cells, and this distinction was independent of maturation stimuli. CD70 was also essential for CD205+ DC function in vivo. Detection of the IL-12–independent IFN-{gamma} pathway was obscured with nontargeted LACK, which was presented by both DC subsets. This in situ analysis points to CD70 as a decision maker for Th1 differentiation by CD205+ DCs, even in Th2-prone BALB/c animals and potentially in vaccine design. The results indicate that two DC subsets have innate propensities to differentially affect the Th1/Th2 balance in vivo and by distinct mechanisms.


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