Capacity of mouse mast cells to prime T cells and to induce specific antibody responses in vivo.

Mouse, human and rat mast cells have been shown to express major histocompatibility complex II molecules and present antigens to specific T-cell hybridomas in vitro. The purpose of our investigation was to determine whether mouse mast cells are able to initiate specific immune responses in vivo. Induction of anti-dinitrophenyl (DNP) immunoglobulin G1 (IgG1) and IgG2a antibodies was performed by transferring ovalbumin (OVA)-DNP-pulsed bone marrow-derived mast cells (BMMC), B cells, or macrophages into naive mice which were boosted later with soluble antigen. Cultured spleen cells from immunized mice were tested for their cytokine content. Our data show that mast cells were by far better inducers of anti-DNP IgG1 antibodies than were B cells and macrophages. In contrast, anti-DNP IgG2a response induced by macrophages was much stronger than that obtained with mast cells whereas B cells were completely unable to elicit this response. In addition to a high index of cell proliferation, spleen cells from mast cell-injected mice produced more interferon-gamma than those mice who received macrophages or B cells by two- to fivefold, and almost 10-fold, respectively. Mast cell-deficient Wf/Wf mice were compared with their normal +/+ littermates and with mast cell-reconstituted Wf/Wf mice to develop delayed-type hypersensitivity (DTH) reactions as well as humoral immune responses. Mast cell sufficient mice as well as mast cell-reconstituted Wf/Wf mice developed significantly increased DTH reactions (P = 0.02, and 0.03, respectively) and higher anti-OVA-specific antibody responses as compared with Wf/Wf mice. Our data suggest that mast cells have the potential to up-regulate both humoral and cellular immune responses in vivo.