Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Bone Marrow Cells / immunology
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Cell Proliferation
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Cell Survival
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Cytokines / genetics
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Cytokines / metabolism
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DNA-Binding Proteins / deficiency*
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DNA-Binding Proteins / immunology
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Dinitrophenols / pharmacology
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Immunoglobulin E / immunology*
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Mast Cells / immunology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Proto-Oncogene Proteins c-bcl-6
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Proto-Oncogene Proteins c-kit / immunology
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RNA, Messenger / metabolism
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Receptors, IgE / immunology*
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Serum Albumin / pharmacology
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Th2 Cells / immunology*
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beta-N-Acetylhexosaminidases / metabolism
Substances
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Antibodies, Monoclonal
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Bcl6 protein, mouse
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Cytokines
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DNA-Binding Proteins
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Dinitrophenols
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Proto-Oncogene Proteins c-bcl-6
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RNA, Messenger
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Receptors, IgE
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Serum Albumin
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dinitrophenyl-human serum albumin conjugate
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Immunoglobulin E
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Proto-Oncogene Proteins c-kit
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beta-N-Acetylhexosaminidases