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 histocompa tibility complex II molecules and present antigens to specific T-cell hybri domas in vitro. The purpose of our investigation was to determine whether m ouse mast cells are able to initiate specific immune responses in vivo. Ind uction of anti-dinitrophenyl (DNP) immunoglobulin G1 (IgG1) and IG2a antibo dies was performed by transferring ovalbumin (OVA)-DNP-pulsed bone marrow-d erived mast cells (BMMC), B cells, or macrophages into naive mice which wer e 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 a nd 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 c ell 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 W-f/W- f mice were compared with their normal +/+ littermates and with mast cell-r econstituted W-f/W-f mice to develop delayed-type hypersensitivity (DTH) re actions as well as humoral immune responses. Mast cell sufficient mice as w ell as mast cell-reconstituted W-f/W-f mice developed significantly increas ed DTH reactions (P=0.02, and 0.03, repectively) and higher anti-OVA-specif ic antibody responses as compared with W-f/W-f mice. Our data suggest that mast cells have the potential to up-regulate both humoral and cellular immu ne responses in vivo.