Bcl6 regulates Th2 type cytokine productions by mast cells activated by FcepsilonRI/IgE cross-linking.

Bcl6-deficient (Bcl6-/-) mice displayed Th2 type inflammation, which caused by abnormality of non-lymphoid cells. However, initiators for the Th2 type inflammation were not clear. In order to elucidate the initiators, we investigated property and function of mast cells derived from Bcl6-/- mice. Mast cells were developed from bone marrow cells cultured with IL-3 (BMMCs). Although the development of BMMCs from Bcl6-/- mice was similar to that from wild-type mice, proliferation of Bcl6-/- BMMCs stimulated with IL-3 was slightly lower than that of wild-type BMMCs. When these BMMCs were stimulated by FcepsilonRI/IgE cross-linking, Bcl6-/- BMMCs produced Th2 cytokines more than wild-type BMMCs did. Thus, Bcl6-/- mast cells are one of the initiators for Th2 type inflammation in Bcl6-/- mice, and Bcl6 may be a molecular target for Th2 type allergic diseases.