| First Author | Ohtsuka Y | Year | 2005 |
| Journal | Mol Immunol | Volume | 42 |
| Issue | 12 | Pages | 1453-9 |
| PubMed ID | 15950739 | Mgi Jnum | J:99053 |
| Mgi Id | MGI:3581006 | Doi | 10.1016/j.molimm.2005.01.011 |
| Citation | Ohtsuka Y, et al. (2005) Bcl6 regulates Th2 type cytokine productions by mast cells activated by FcvarepsilonRI/IgE cross-linking. Mol Immunol 42(12):1453-1459 |
| abstractText | 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 FcvarepsilonRI/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. |
