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* Experimental Immunology Branch, National Cancer Institute and
Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892; and
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853
The cytokines secreted by pathogen-activated human dendritic cells (DC) are strongly regulated in vitro by histamine, a major component of mast cell granules, ultimately modulating the capacity of the DC to polarize naive T cells. Because DC and mast cells are located in close proximity in peripheral compartments, we hypothesized that mast cell products would influence the maturation of DC and hence the Th balance of an immune response in vivo. In this study, we show that specific mast cell degranulation stimuli, given s.c. in mice with Ag and adjuvant, produce effector T cells that proliferate to Ag but secrete dramatically reduced levels of IFN-
and increased amounts of IL-4 compared with control T cells primed in the absence of a mast cell stimulus. Immunization with Ag and adjuvant in the presence of a degranulation stimulus also resulted in the accumulation of DC in the draining lymph nodes that had reduced capacity to induce Ag-specific Th1 cells, in comparison with DC from mice lacking a degranulation stimulus. Therefore, by acting upon DC at sites of inflammation, mast cells play a critical role in determining the polarity of Ag-specific T cell responses in vivo.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported in part by the Intramural Research Program of the National Institutes of Health (NIH) (National Cancer Institute) and in part by an appointment to the Oak Ridge Institute for Science and Education’s (ORISE) Research Associates Program at the NIH. The program is administered by ORISE through an interagency agreement between the U.S. Department of Energy and the NIH.
2 Address correspondence and reprint requests to Dr. David M. Segal, Experimental Immunology Branch, National Institutes of Health, Building 10, Room 4B36, 9000 Rockville Pike, Bethesda, MD 20892. E-mail address: dave_segal{at}nih.gov
3 Abbreviations used in this paper: DC, dendritic cell; ODN, oligodeoxynucleotide; TNP, trinitrophenyl.
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